The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.
Highly differentiated epithelial cells of the visceral layer of BOWMAN CAPSULE of the KIDNEY. They are composed of a cell body with major CELL SURFACE EXTENSIONS and secondary fingerlike extensions called pedicels. They enwrap the KIDNEY GLOMERULUS capillaries with their cell surface extensions forming a filtration structure. The pedicels of neighboring podocytes interdigitate with each other leaving between them filtration slits that are bridged by an extracellular structure impermeable to large macromolecules called the slit diaphragm, and provide the last barrier to protein loss in the KIDNEY.
A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
A type of glomerulonephritis that is characterized by the accumulation of immune deposits (COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane.
Pathological processes of the KIDNEY or its component tissues.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.
Pathological processes of the KIDNEY without inflammatory or neoplastic components. Nephrosis may be a primary disorder or secondary complication of other diseases. It is characterized by the NEPHROTIC SYNDROME indicating the presence of PROTEINURIA and HYPOALBUMINEMIA with accompanying EDEMA.
Creatinine is a waste product that's generated from muscle metabolism, typically filtered through the kidneys and released in urine, with increased levels in blood indicating impaired kidney function.
PUROMYCIN derivative that lacks the methoxyphenylalanyl group on the amine of the sugar ring. It is an antibiotic with antineoplastic properties and can cause nephrosis.
The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to INULIN clearance.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
Examination of urine by chemical, physical, or microscopic means. Routine urinalysis usually includes performing chemical screening tests, determining specific gravity, observing any unusual color or odor, screening for bacteriuria, and examining the sediment microscopically.
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.
Inflammation of any part of the KIDNEY.
Presence of blood in the urine.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
Laboratory tests used to evaluate how well the kidneys are working through examination of blood and urine.
A kidney disease with no or minimal histological glomerular changes on light microscopy and with no immune deposits. It is characterized by lipid accumulation in the epithelial cells of KIDNEY TUBULES and in the URINE. Patients usually show NEPHROTIC SYNDROME indicating the presence of PROTEINURIA with accompanying EDEMA.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
The layer of EXTRACELLULAR MATRIX that lies between the ENDOTHELIUM of the glomerular capillaries and the PODOCYTES of the inner or visceral layer of the BOWMAN CAPSULE. It is the product of these two cell types. It acts as a physical barrier and an ion-selective filter.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Excision of kidney.
Renal syndrome in human immunodeficiency virus-infected patients characterized by nephrotic syndrome, severe proteinuria, focal and segmental glomerulosclerosis with distinctive tubular and interstitial changes, enlarged kidneys, and peculiar tubuloreticular structures. The syndrome is distinct from heroin-associated nephropathy as well as other forms of kidney disease seen in HIV-infected patients.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
The transference of a kidney from one human or animal to another.
A complication of PREGNANCY, characterized by a complex of symptoms including maternal HYPERTENSION and PROTEINURIA with or without pathological EDEMA. Symptoms may range between mild and severe. Pre-eclampsia usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
A specialized barrier in the kidney, consisting of the fenestrated CAPILLARY ENDOTHELIUM; GLOMERULAR BASEMENT MEMBRANE; and glomerular epithelium (PODOCYTES). The barrier prevents the filtration of PLASMA PROTEINS.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)
Narrow pieces of material impregnated or covered with a substance used to produce a chemical reaction. The strips are used in detecting, measuring, producing, etc., other substances. (From Dorland, 28th ed)
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.
A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.
Inbred NZB mice are a strain of laboratory mice that spontaneously develop an autoimmune disease similar to human systemic lupus erythematosus (SLE), characterized by the production of autoantibodies, immune complex deposition, and glomerulonephritis.
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.
A darkly stained mat-like EXTRACELLULAR MATRIX (ECM) that separates cell layers, such as EPITHELIUM from ENDOTHELIUM or a layer of CONNECTIVE TISSUE. The ECM layer that supports an overlying EPITHELIUM or ENDOTHELIUM is called basal lamina. Basement membrane (BM) can be formed by the fusion of either two adjacent basal laminae or a basal lamina with an adjacent reticular lamina of connective tissue. BM, composed mainly of TYPE IV COLLAGEN; glycoprotein LAMININ; and PROTEOGLYCAN, provides barriers as well as channels between interacting cell layers.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Elements of limited time intervals, contributing to particular results or situations.
An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A condition in which albumin level in blood (SERUM ALBUMIN) is below the normal range. Hypoalbuminemia may be due to decreased hepatic albumin synthesis, increased albumin catabolism, altered albumin distribution, or albumin loss through the urine (ALBUMINURIA).
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
An LDL-RECEPTOR RELATED PROTEIN found in the neuroepithelium and in proximal tubular cells of the kidney. It is considered a multiligand receptor in that it binds to a variety of ligands with relatively high affinity and may function in mediating the uptake and lysosomal degradation of macromolecules such as: LIPOPROTEINS; ENDOPEPTIDASES; and PROTEASE INHIBITORS.
An antibiotic substance derived from Penicillium stoloniferum, and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase. Mycophenolic acid is important because of its selective effects on the immune system. It prevents the proliferation of T-cells, lymphocytes, and the formation of antibodies from B-cells. It also may inhibit recruitment of leukocytes to inflammatory sites. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1301)
A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.
A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA-containing IMMUNE COMPLEXES within the blood vessels throughout the body, including those in the kidney (KIDNEY GLOMERULUS). Clinical symptoms include URTICARIA; ERYTHEMA; ARTHRITIS; GASTROINTESTINAL HEMORRHAGE; and renal involvement. Most cases are seen in children after acute upper respiratory infections.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
An abnormal protein with unusual thermosolubility characteristics that is found in the urine of patients with MULTIPLE MYELOMA.
An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
Hardening of the KIDNEY due to infiltration by fibrous connective tissue (FIBROSIS), usually caused by renovascular diseases or chronic HYPERTENSION. Nephrosclerosis leads to renal ISCHEMIA.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Tetrazoles are heterocyclic organic compounds containing a 1,3,5-triazole ring with an additional nitrogen atom, often used in pharmaceuticals as bioisosteres for carboxylic acid groups due to their isoelectronic nature and similar hydrogen bonding capabilities.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Therapy with two or more separate preparations given for a combined effect.
Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
The thin membranous structure supporting the adjoining glomerular capillaries. It is composed of GLOMERULAR MESANGIAL CELLS and their EXTRACELLULAR MATRIX.
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
The renal tubule portion that extends from the BOWMAN CAPSULE in the KIDNEY CORTEX into the KIDNEY MEDULLA. The proximal tubule consists of a convoluted proximal segment in the cortex, and a distal straight segment descending into the medulla where it forms the U-shaped LOOP OF HENLE.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney.
A condition in pregnant women with elevated systolic (>140 mm Hg) and diastolic (>90 mm Hg) blood pressure on at least two occasions 6 h apart. HYPERTENSION complicates 8-10% of all pregnancies, generally after 20 weeks of gestation. Gestational hypertension can be divided into several broad categories according to the complexity and associated symptoms, such as EDEMA; PROTEINURIA; SEIZURES; abnormalities in BLOOD COAGULATION and liver functions.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
Laboratory rats that have been produced from a genetically manipulated rat EGG or rat EMBRYO, MAMMALIAN. They contain genes from another species.
Serum proteins that have the most rapid migration during ELECTROPHORESIS. This subgroup of globulins is divided into faster and slower alpha(1)- and alpha(2)-globulins.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
'Rats, Inbred Lew' is a strain of laboratory rat that is widely used in biomedical research, known for its consistent genetic background and susceptibility to certain diseases, which makes it an ideal model for studying the genetic basis of complex traits and disease processes.
A group of inherited conditions characterized initially by HEMATURIA and slowly progressing to RENAL INSUFFICIENCY. The most common form is the Alport syndrome (hereditary nephritis with HEARING LOSS) which is caused by mutations in genes for TYPE IV COLLAGEN and defective GLOMERULAR BASEMENT MEMBRANE.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.
A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).

Angiotensin-converting enzyme is upregulated in the proximal tubules of rats with intense proteinuria. (1/3373)

Persistent proteinuria is considered a deleterious prognostic factor in most progressive renal diseases. However, the mechanisms by which proteinuria induces renal damage remain undetermined. Since proximal tubular cells possess all the machinery to generate angiotensin II (Ang II), we approached the hypothesis that proteinuria could elicit the renal activation of the renin-angiotensin system in a model of intense proteinuria and interstitial nephritis induced by protein overload. After uninephrectomy (UNX), Wistar-Kyoto rats received daily injections of 1 g BSA or saline for 8 days. The mean peak of proteinuria was observed at the fourth day (538+/-89 versus 3+/-1 mg/24 h in UNX controls; n=12; P<0.05) and was increased during the whole study period (at the eighth day: 438+/-49 mg/24 h; n=12; P=NS). Morphological examination of the kidneys at the end of the study showed marked tubular lesions (atrophy, vacuolization, dilation, and casts), interstitial infiltration of mononuclear cells, and mesangial expansion. In relation to UNX control rats, renal cortex of BSA-overloaded rats showed an increment in the gene expression of angiotensinogen (2.4-fold) and angiotensin-converting enzyme (ACE) (2.1-fold), as well as a diminution in renin gene expression. No changes were observed in angiotensin type 1 (AT1) receptor mRNA expression in both groups of rats. By in situ reverse transcription-polymerase chain reaction and immunohistochemistry, ACE expression (gene and protein) was mainly localized in proximal and distal tubules and in the glomeruli. By immunohistochemistry, angiotensinogen was localized only in proximal tubules, and AT1 receptor was localized mainly in proximal and distal tubules. In the tubular brush border, an increase in ACE activity was also seen (5. 5+/-0.5 versus 3.1+/-0.7 U/mg protein x10(-4) in UNX control; n=7; P<0.05). Our results show that in the kidney of rats with intense proteinuria, ACE and angiotensinogen were upregulated, while gene expression of renin was inhibited and AT1 was unmodified. On the whole, these data suggest an increase in Ang II intrarenal generation. Since Ang II can elicit renal cell growth and matrix production through the activation of AT1 receptor, this peptide may be responsible for the tubulointerstitial lesions occurring in this model. These results suggest a novel mechanism by which proteinuria may participate in the progression of renal diseases.  (+info)

Up-regulation of glomerular extracellular matrix and transforming growth factor-beta expression in RF/J mice. (2/3373)

BACKGROUND: RF/J mice were first reported as a murine model of spontaneous glomerulosclerosis by Gude and Lupton in 1960, but the precise histologic characteristics and immunopathological background of this mouse have not been investigated further. METHODS: Measurements of serum levels of immunoglobulins, anti-single strand DNA (anti-ss-DNA) antibody, complement (C3), and circulating immune complex (IC) were performed. Analyses of glomerular histological and immunopathological lesions in association with the detection of mRNA expression of collagen IV, TGF-beta, matrix protein turnover related enzymes, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2) and platelet-derived growth factor (PDGF) were also performed in young (10-week-old) and elderly (60-week-old) RF/J mice with age-matched BALB/C mice as the controls. RESULTS: High levels of serum IgA and IgG from as early as 20 weeks of age were noted in the RF/J mice. Serum anti-ss-DNA antibody of aged RF/J mice increased up to 23% of that of aged MRL-lpr/lpr mice, and serum C3 concentration significantly decreased with age, reaching lower levels than that of BALB/c mice. IgA-IC levels were significantly high compared to BALB/C mice both in the early and late stages of life, whereas IgG-IC levels were high only in mice younger than 20 weeks. Semiquantitative and quantitative analyzes of renal histopathological findings revealed significantly marked and age-related mesangial matrix expansion in RF/J mice, with increasing frequency of global glomerular sclerosis and tubulointerstitial damage. On the other hand, although precise measurements of glomerular cell numbers also showed an apparent augmentation in both young and old RF/J mice compared to BALB/C mice, glomerular cellularity decreased with age in RF/J mice. Immunohistochemical study revealed massive immunoglobulin deposition from a young age in association with significantly higher accumulation of matrix proteins, such as types I and IV collagen and laminin from the early stage of life. In addition, in these glomeruli, transforming growth factor-beta1 (TGF-beta1) was highly expressed both in young and old mice. The mRNA expression of MMP-2 was up-regulated only in the early stage of life. Although PDGF mRNA of RF/J mice was significantly up-regulated in the early stage of life, the differences between the mice disappeared in the late stage of life. CONCLUSIONS: These findings suggest that in RF/J mice, an immunopathological background inducing high serum immunoglobulin and IC levels from the early stage of life is closely related to mesangioproliferative glomerular lesions mediated by PDGF, and that development of massive extracellular matrix accumulation in glomeruli was induced by up-regulated expression of TGF-beta with inappropriate regulation of protein turnover-related enzyme production.  (+info)

Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis. (3/3373)

BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN.  (+info)

Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy. (4/3373)

BACKGROUND: Proteinuria and tubular atrophy have both been closely linked with progressive renal failure. We hypothesized that apoptosis may be induced by tubular cell exposure to heavy proteinuria, potentially leading to tubular atrophy. Apoptosis was studied in a rat model of "pure" proteinuria, which does not induce renal impairment, namely protein-overload proteinuria. METHODS: Adult female Lewis rats underwent intraperitoneal injection of 2 g of bovine serum albumin (BSA, N = 16) or sham saline injections (controls, N = 8) daily for seven days. Apoptosis was assessed at day 7 in tissue sections using in situ end labeling (ISEL) and electron microscopy. ISEL-positive nuclei (apoptotic particles) were counted in blinded fashion using image analysis with NIH Image. Cell proliferation was assessed by detection of mRNA for histone by in situ hybridization, followed by counting of positive cells using NIH Image. RESULTS: Animals injected with saline showed very low levels of apoptosis on image analysis. BSA-injected rats had heavy proteinuria and showed both cortical and medullary apoptosis on ISEL. This was predominantly seen in the tubules and, to a lesser extent, in the interstitial compartment. Overall, the animals injected with BSA showed a significant 30-fold increase in the number of cortical apoptotic particles. Electron microscopy of tubular cells in a BSA-injected animal showed a progression of ultrastructural changes consistent with tubular cell apoptosis. The BSA-injected animals also displayed a significant increase in proximal tubular cell proliferation. This increased proliferation was less marked than the degree of apoptosis. CONCLUSION: Protein-overload proteinuria in rats induces tubular cell apoptosis. This effect is only partially balanced by proliferation and potentially provides a direct mechanism whereby heavy proteinuria can induce tubular atrophy and progressive renal failure.  (+info)

Mycophenolate mofetil prevents the progressive renal failure induced by 5/6 renal ablation in rats. (5/3373)

BACKGROUND: Extensive renal ablation is associated with progressive sclerosis of the remnant kidney. Because lymphocytes and monocytes accumulate in the remnant kidney, it is likely that they play a role in the renal scarring. Therefore, we treated rats with 5/6 nephrectomy (5/6Nx) with mycophenolate mofetil (MMF), a drug that has an antiproliferative effect and that suppresses the expression of intercellular adhesion molecules. METHODS: Sprague-Dawley rats with 5/6Nx received MMF (30 mg. kg-1. day-1 by daily gastric gavage, N = 15) or vehicle (N = 16). Ten additional rats were sham operated. All rats were fed a 30% protein diet. Body weight, serum creatinine, and urinary protein excretion were determined weekly. Lipid peroxidation, as a measure of oxidative stress observed by urinary malondialdehyde determinations, was performed every two weeks. Histologic studies were done in the remnant kidney four weeks (9 rats from the vehicle-treated group, 7 rats from the MMF group, and 5 sham-operated rats) and eight weeks after surgery (the remaining rats). Glomerular volume, sclerosis in glomeruli (segmental and global) and interstitium (semiquantitative scale), infiltrating lymphocytes and macrophages (CD43- and ED1-positive cells), and expression of adhesion molecules (CD54, CD18, and CD11b) were analyzed. RESULTS: MMF treatment prevented the progressive increment in serum creatinine and the proteinuria observed in the 5/6 nephrectomized rats during the eight weeks of observation (P < 0.01). Weight gain was comparable in the MMF-treated and sham-operated rats, whereas weight gain was decreased in untreated 5/6 nephrectomized rats. Excretion of malondialdehyde increased after surgery but returned sooner to control levels in the MMF-treated rats. Increments in glomerular size and mean arterial blood pressure induced by renal ablation were not modified by MMF treatment. Eight weeks after surgery, segmental sclerosis was present in 48.4 +/- 8.35% (+/- sd) glomeruli in the vehicle-treated group versus 25 +/- 10.5% in the MMF-treated group (P < 0.001). Interstitial fibrosis was reduced significantly with MMF treatment (P < 0.001). Infiltration with CD43- and ED1-positive cells in glomeruli and interstitium was two to five times lower in MMF-treated rats (P < 0.01). Expression of adhesion molecules CD18 and CD11b was similarly reduced. CONCLUSION: MMF ameliorates the progressive renal damage in the remnant kidney after 5/6Nx. This effect is associated with a reduction in the infiltration of lymphocytes and monocytes, whereas glomerular hypertrophy and systemic hypertension are unchanged.  (+info)

HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection. (6/3373)

BACKGROUND: Human immunodeficiency virus-associated nephropathy (HIVAN) can be the initial presentation of HIV-1 infection. As a result, many have assumed that HIVAN can occur at any point in the infection. This issue has important implications for appropriate therapy and, perhaps, for pathogenesis. Since the development of new case definitions for acquired immunodeficiency syndrome (AIDS) and better tools to assess infection, the relationship of HIVAN to the time of AIDS infection has not been addressed. In this study, we reassessed the stage of infection at the time of HIVAN diagnosis in 10 patients, and we reviewed all previously published cases applying the new case definitions to assess stage of infection. METHODS: HIVAN was confirmed by kidney biopsy in HIV seropositive patients with azotemia and/or proteinuria. CD4+ cell count and plasma HIV-1 RNA copy number were measured. We also reviewed all published cases of HIVAN to determine if AIDS-defining conditions, by current Centers for Disease Control definitions, were present in patients with biopsy-proven HIVAN. RESULTS: Twenty HIV-1 seropositive patients with proteinuria and an elevated creatinine concentration were biopsied. HIVAN was the single most common cause of renal disease. CD4+ cell count was below 200/mm3 in all patients with HIVAN, fulfilling Centers for Disease Control criteria for an AIDS-defining condition. HIV-1 plasma RNA was detectable in all patients with HIVAN. In reviewing previous reports, an AIDS-defining condition was present in virtually all patients with HIVAN. CONCLUSION: HIVAN develops late, not early, in the course of HIV-1 infection following the development of AIDS. This likely accounts for the poor prognosis noted in previous publications and has implications for pathogenesis. In addition, given the detectable viral RNA levels, highly active antiretroviral therapy is indicated in HIVAN. Highly active antiretroviral therapy may improve survival as well as alter the natural history of HIVAN.  (+info)

Long-term effects of cyclosporine A in Alport's syndrome. (7/3373)

BACKGROUND: In 1991, our initial results of cyclosporine A (CsA) administration in eight patients with Alport's syndrome were published. A significant decrease in or disappearance of proteinuria and apparently good tolerance to CsA were observed in all patients. METHODS: CsA administration has been maintained in these eight patients with the aim of obtaining further information about the clinical course of the disease. The ages of these eight patients currently range from 15 to 27 years, and the mean duration of treatment is from 7 to 10 years (x = 8.4 years). RESULTS: Renal function has remained stable, with no evaluable changes in serum creatinine levels compared with pre-CsA treatment values. Proteinuria in all patients has either remained negative or are values far lower than pretreatment levels. A second renal biopsy was performed in all patients after five years of CsA administration. No aggravation of the lesion present at the first biopsy or lesions typical of cyclosporine intoxication was observed. CONCLUSIONS: After a mean duration of 8.4 years and with no deterioration in renal function, we found possible beneficial effects of the continued treatment of CsA in patients with Alport's syndrome who present evidence of progression to renal insufficiency.  (+info)

Circulating vascular endothelial growth factor is not increased during relapses of steroid-sensitive nephrotic syndrome. (8/3373)

BACKGROUND: An uncharacterized circulating factor that increases vascular permeability has previously been described in childhood steroid-sensitive nephrotic syndrome (SSNS). The aim of this study was to determine whether this factor is vascular endothelial growth factor (VEGF), the recently described endothelial cell mitogen and enhancer of vascular permeability. METHODS: Plasma and urine VEGF levels were measured in children with SSNS in both relapse and remission and in normal age- and sex-matched controls. Semiquantitative reverse transcriptase-polymerase chain reaction studies investigating VEGF mRNA expression were performed on peripheral blood mononuclear cells isolated from children with SSNS in relapse and controls. In two experimental models (one-hour and three-day follow-up postinfusion), Sprague-Dawley rats were intravenously administered 50 microg rVEGF to determine whether this induced either proteinuria or glomerular histologic change. RESULTS: Plasma VEGF levels and urine VEGF/creatinine ratios were not elevated in SSNS relapse compared with remission and control samples. Peripheral blood mononuclear cell VEGF mRNA expression was no different in SSNS patients compared with controls. The administration of VEGF to rats induced an acute reversible fall in systemic blood pressure but did not result in the development of either proteinuria or glomerular histologic change. CONCLUSION: Increased circulating VEGF levels are not responsible for the proteinuria observed during relapses of SSNS. Further studies are warranted to investigate intrarenal VEGF expression.  (+info)

Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.

However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.

The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.

A kidney glomerulus is a functional unit in the nephron of the kidney. It is a tuft of capillaries enclosed within a structure called Bowman's capsule, which filters waste and excess fluids from the blood. The glomerulus receives blood from an afferent arteriole and drains into an efferent arteriole.

The process of filtration in the glomerulus is called ultrafiltration, where the pressure within the glomerular capillaries drives plasma fluid and small molecules (such as ions, glucose, amino acids, and waste products) through the filtration membrane into the Bowman's space. Larger molecules, like proteins and blood cells, are retained in the blood due to their larger size. The filtrate then continues down the nephron for further processing, eventually forming urine.

Nephrotic syndrome is a group of symptoms that indicate kidney damage, specifically damage to the glomeruli—the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. The main features of nephrotic syndrome are:

1. Proteinuria (excess protein in urine): Large amounts of a protein called albumin leak into the urine due to damaged glomeruli, which can't properly filter proteins. This leads to low levels of albumin in the blood, causing fluid buildup and swelling.
2. Hypoalbuminemia (low blood albumin levels): As albumin leaks into the urine, the concentration of albumin in the blood decreases, leading to hypoalbuminemia. This can cause edema (swelling), particularly in the legs, ankles, and feet.
3. Edema (fluid retention and swelling): With low levels of albumin in the blood, fluids move into the surrounding tissues, causing swelling or puffiness. The swelling is most noticeable around the eyes, face, hands, feet, and abdomen.
4. Hyperlipidemia (high lipid/cholesterol levels): The kidneys play a role in regulating lipid metabolism. Damage to the glomeruli can lead to increased lipid production and high cholesterol levels in the blood.

Nephrotic syndrome can result from various underlying kidney diseases, such as minimal change disease, membranous nephropathy, or focal segmental glomerulosclerosis. Treatment depends on the underlying cause and may include medications to control inflammation, manage high blood pressure, and reduce proteinuria. In some cases, dietary modifications and lifestyle changes are also recommended.

Podocytes are specialized cells that make up the visceral epithelial layer of the glomerular basement membrane in the kidney. They have long, interdigitating foot processes that wrap around the capillaries of the glomerulus and play a crucial role in maintaining the filtration barrier of the kidney. The slit diaphragms between the foot processes allow for the passage of small molecules while retaining larger proteins in the bloodstream. Podocytes also contribute to the maintenance and regulation of the glomerular filtration rate, making them essential for normal renal function. Damage or loss of podocytes can lead to proteinuria and kidney disease.

Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury that involves scarring or sclerosis in some (segmental) areas of some (focal) glomeruli. Glomeruli are the tiny blood vessel clusters within the kidneys that filter waste and excess fluids from the blood.

In FSGS, the scarring occurs due to damage to the glomerular basement membrane, which can be caused by various factors such as genetic mutations, viral infections, or immune system disorders. The damage leads to the accumulation of extracellular matrix proteins and the formation of scar tissue, impairing the kidney's ability to filter blood effectively.

FSGS is characterized by proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and declining kidney function, which can lead to end-stage renal disease if left untreated. The focal and segmental nature of the scarring means that not all glomeruli are affected, and only some areas of each affected glomerulus are damaged, making FSGS a highly variable condition with different clinical presentations and outcomes.

Glomerulonephritis is a medical condition that involves inflammation of the glomeruli, which are the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. This inflammation can impair the kidney's ability to filter blood properly, leading to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), hypertension (high blood pressure), and eventually kidney failure.

Glomerulonephritis can be acute or chronic, and it may occur as a primary kidney disease or secondary to other medical conditions such as infections, autoimmune disorders, or vasculitis. The diagnosis of glomerulonephritis typically involves a combination of medical history, physical examination, urinalysis, blood tests, and imaging studies, with confirmation often requiring a kidney biopsy. Treatment depends on the underlying cause and severity of the disease but may include medications to suppress inflammation, control blood pressure, and manage symptoms.

Membranous glomerulonephritis (MGN) is a kidney disorder that leads to the inflammation and damage of the glomeruli, which are the tiny blood vessels in the kidneys responsible for filtering waste and excess fluids from the blood. In MGN, the membrane that surrounds the glomerular capillaries becomes thickened and damaged due to the deposit of immune complexes, primarily composed of antibodies and antigens.

The onset of membranous glomerulonephritis can be either primary (idiopathic) or secondary to various underlying conditions such as autoimmune diseases (like systemic lupus erythematosus), infections (hepatitis B or C, syphilis, endocarditis), medications, or malignancies.

The symptoms of membranous glomerulonephritis may include:

1. Proteinuria - the presence of excess protein, specifically albumin, in the urine. This can lead to nephrotic syndrome, characterized by heavy protein loss in urine, edema (swelling), hypoalbuminemia (low blood albumin levels), and hyperlipidemia (high blood lipid levels).
2. Hematuria - the presence of red blood cells in the urine, which can be visible or microscopic.
3. Hypertension - high blood pressure.
4. Edema - swelling in various body parts due to fluid retention.
5. Nephrotic range proteinuria (protein loss greater than 3.5 grams per day) and/or nephritic syndrome (a combination of hematuria, proteinuria, hypertension, and kidney dysfunction) can be observed in some cases.

The diagnosis of membranous glomerulonephritis typically involves a thorough medical history, physical examination, urinalysis, blood tests, and imaging studies. A definitive diagnosis often requires a kidney biopsy to assess the glomerular structure and the nature of the immune complex deposits. Treatment depends on the underlying cause and severity of the disease and may include corticosteroids, immunosuppressants, blood pressure management, and supportive care for symptoms like edema and proteinuria.

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

IGA glomerulonephritis (also known as Berger's disease) is a type of glomerulonephritis, which is a condition characterized by inflammation of the glomeruli, the tiny filtering units in the kidneys. In IgA glomerulonephritis, the immune system produces an abnormal amount of IgA antibodies, which deposit in the glomeruli and cause inflammation. This can lead to symptoms such as blood in the urine, protein in the urine, and swelling in the legs and feet. In some cases, it can also lead to kidney failure. The exact cause of IgA glomerulonephritis is not known, but it is often associated with other conditions such as infections, autoimmune diseases, and certain medications.

Nephrosis is an older term that was used to describe a group of kidney diseases, primarily characterized by the damage and loss of function in the glomeruli - the tiny filtering units within the kidneys. This results in the leakage of large amounts of protein (primarily albumin) into the urine, a condition known as proteinuria.

The term "nephrosis" was often used interchangeably with "minimal change nephropathy," which is a specific type of kidney disorder that demonstrates little to no changes in the glomeruli under a microscope, despite significant protein leakage. However, current medical terminology and classifications prefer the use of more precise terms to describe various kidney diseases, such as minimal change disease, focal segmental glomerulosclerosis, or membranous nephropathy, among others.

It is important to consult with a healthcare professional or refer to updated medical resources for accurate and current information regarding kidney diseases and their specific diagnoses.

Creatinine is a waste product that's produced by your muscles and removed from your body by your kidneys. Creatinine is a breakdown product of creatine, a compound found in meat and fish, as well as in the muscles of vertebrates, including humans.

In healthy individuals, the kidneys filter out most of the creatinine and eliminate it through urine. However, when the kidneys are not functioning properly, creatinine levels in the blood can rise. Therefore, measuring the amount of creatinine in the blood or urine is a common way to test how well the kidneys are working. High creatinine levels in the blood may indicate kidney damage or kidney disease.

Puromycin aminonucleoside is not a medical condition, but rather a laboratory reagent used in research. It is a synthetic antibiotic and analogue of the amino acid tyrosine, which specifically inhibits protein synthesis in eukaryotic cells by interacting with the peptidyl transferase center of the 60S ribosomal subunit. This compound has been widely used as a tool to study various cellular processes, including programmed cell death (apoptosis), autophagy, and lysosome biogenesis. Prolonged exposure to puromycin aminonucleoside can induce cytopathic effects, such as vacuolization and detachment of cells, which are often used as markers for its effectiveness in inhibiting protein synthesis.

Glomerular filtration rate (GFR) is a test used to check how well the kidneys are working. Specifically, it estimates how much blood passes through the glomeruli each minute. The glomeruli are the tiny fibers in the kidneys that filter waste from the blood. A lower GFR number means that the kidneys aren't working properly and may indicate kidney disease.

The GFR is typically calculated using a formula that takes into account the patient's serum creatinine level, age, sex, and race. The most commonly used formula is the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation. A normal GFR is usually above 90 mL/min/1.73m2, but this can vary depending on the individual's age and other factors.

Diabetic nephropathy is a kidney disease that occurs as a complication of diabetes. It is also known as diabetic kidney disease (DKD). This condition affects the ability of the kidneys to filter waste and excess fluids from the blood, leading to their accumulation in the body.

Diabetic nephropathy is caused by damage to the small blood vessels in the kidneys, which can occur over time due to high levels of glucose in the blood. This damage can lead to scarring and thickening of the kidney's filtering membranes, reducing their ability to function properly.

Symptoms of diabetic nephropathy may include proteinuria (the presence of protein in the urine), edema (swelling in the legs, ankles, or feet due to fluid retention), and hypertension (high blood pressure). Over time, if left untreated, diabetic nephropathy can progress to end-stage kidney disease, which requires dialysis or a kidney transplant.

Preventing or delaying the onset of diabetic nephropathy involves maintaining good control of blood sugar levels, keeping blood pressure under control, and making lifestyle changes such as quitting smoking, eating a healthy diet, and getting regular exercise. Regular monitoring of kidney function through urine tests and blood tests is also important for early detection and treatment of this condition.

Urinalysis is a medical examination and analysis of urine. It's used to detect and manage a wide range of disorders, such as diabetes, kidney disease, and liver problems. A urinalysis can also help monitor medications and drug compliance. The test typically involves checking the color, clarity, and specific gravity (concentration) of urine. It may also include chemical analysis to detect substances like glucose, protein, blood, and white blood cells, which could indicate various medical conditions. In some cases, a microscopic examination is performed to identify any abnormal cells, casts, or crystals present in the urine.

Albuminuria is a medical condition that refers to the presence of albumin in the urine. Albumin is a type of protein normally found in the blood, but not in the urine. When the kidneys are functioning properly, they prevent large proteins like albumin from passing through into the urine. However, when the kidneys are damaged or not working correctly, such as in nephrotic syndrome or other kidney diseases, small amounts of albumin can leak into the urine.

The amount of albumin in the urine is often measured in milligrams per liter (mg/L) or in a spot urine sample, as the albumin-to-creatinine ratio (ACR). A small amount of albumin in the urine is called microalbuminuria, while a larger amount is called macroalbuminuria or proteinuria. The presence of albuminuria can indicate kidney damage and may be a sign of underlying medical conditions such as diabetes or high blood pressure. It is important to monitor and manage albuminuria to prevent further kidney damage and potential complications.

Nephritis is a medical term that refers to inflammation of the kidneys, specifically affecting the glomeruli - the tiny filtering units inside the kidneys. The condition can cause damage to the glomeruli, leading to impaired kidney function and the leakage of protein and blood into the urine.

Nephritis can result from a variety of causes, including infections, autoimmune disorders, and exposure to certain medications or toxins. Depending on the severity and underlying cause, nephritis may be treated with medications, dietary modifications, or other therapies aimed at reducing inflammation and preserving kidney function. In severe cases, hospitalization and more intensive treatments may be necessary.

Hematuria is a medical term that refers to the presence of blood in urine. It can be visible to the naked eye, which is called gross hematuria, or detected only under a microscope, known as microscopic hematuria. The blood in urine may come from any site along the urinary tract, including the kidneys, ureters, bladder, or urethra. Hematuria can be a symptom of various medical conditions, such as urinary tract infections, kidney stones, kidney disease, or cancer of the urinary tract. It is essential to consult a healthcare professional if you notice blood in your urine to determine the underlying cause and receive appropriate treatment.

Lupus nephritis is a type of kidney inflammation (nephritis) that can occur in people with systemic lupus erythematosus (SLE), an autoimmune disease. In lupus nephritis, the immune system produces abnormal antibodies that attack the tissues of the kidneys, leading to inflammation and damage. The condition can cause a range of symptoms, including proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and eventually kidney failure if left untreated. Lupus nephritis is typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment may include medications to suppress the immune system and control inflammation, such as corticosteroids and immunosuppressive drugs.

Membranoproliferative Glomerulonephritis (MPGN) is a type of glomerulonephritis, which is a group of kidney disorders characterized by inflammation and damage to the glomeruli, the tiny blood vessels in the kidneys responsible for filtering waste and excess fluids from the blood.

MPGN is specifically characterized by thickening of the glomerular basement membrane and proliferation (increased number) of cells in the mesangium, a region within the glomerulus. This condition can be primary or secondary to other diseases such as infections, autoimmune disorders, or monoclonal gammopathies.

MPGN is typically classified into three types based on the pattern of injury seen on electron microscopy: Type I, Type II (Dense Deposit Disease), and Type III. Each type has distinct clinical features, laboratory findings, and treatment approaches. Symptoms of MPGN may include hematuria (blood in urine), proteinuria (protein in urine), hypertension (high blood pressure), edema (swelling), and eventually progress to chronic kidney disease or end-stage renal disease if left untreated.

Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.

CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.

Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.

Kidney function tests (KFTs) are a group of diagnostic tests that evaluate how well your kidneys are functioning by measuring the levels of various substances in the blood and urine. The tests typically assess the glomerular filtration rate (GFR), which is an indicator of how efficiently the kidneys filter waste from the blood, as well as the levels of electrolytes, waste products, and proteins in the body.

Some common KFTs include:

1. Serum creatinine: A waste product that's produced by normal muscle breakdown and is excreted by the kidneys. Elevated levels may indicate reduced kidney function.
2. Blood urea nitrogen (BUN): Another waste product that's produced when protein is broken down and excreted by the kidneys. Increased BUN levels can suggest impaired kidney function.
3. Estimated glomerular filtration rate (eGFR): A calculation based on serum creatinine, age, sex, and race that estimates the GFR and provides a more precise assessment of kidney function than creatinine alone.
4. Urinalysis: An examination of a urine sample to detect abnormalities such as protein, blood, or bacteria that may indicate kidney disease.
5. Electrolyte levels: Measurement of sodium, potassium, chloride, and bicarbonate in the blood to ensure they're properly balanced, which is essential for normal kidney function.

KFTs are often ordered as part of a routine check-up or when kidney disease is suspected based on symptoms or other diagnostic tests. Regular monitoring of kidney function can help detect and manage kidney disease early, potentially preventing or slowing down its progression.

Lipoid nephrosis is a historical term for a kidney disorder now more commonly referred to as minimal change disease (MCD). It is a type of glomerulonephritis which is characterized by the loss of proteins in the urine (proteinuria) due to damage to the glomeruli, the tiny filtering units within the kidneys.

The term "lipoid" refers to the presence of lipids or fats in the glomeruli, which can be observed under a microscope. However, it's worth noting that not all cases of MCD involve lipid accumulation in the glomeruli.

MCD is typically idiopathic, meaning its cause is unknown, but it can also occur as a secondary condition related to other medical disorders such as allergies, infections, or medications. It primarily affects children, but can also occur in adults. Treatment usually involves corticosteroids and other immunosuppressive therapies to control proteinuria and prevent kidney damage.

Angiotensin-Converting Enzyme (ACE) inhibitors are a class of medications that are commonly used to treat various cardiovascular conditions, such as hypertension (high blood pressure), heart failure, and diabetic nephropathy (kidney damage in people with diabetes).

ACE inhibitors work by blocking the action of angiotensin-converting enzyme, an enzyme that converts the hormone angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels and increases blood pressure. By inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to relax and widen, which lowers blood pressure and reduces the workload on the heart.

Some examples of ACE inhibitors include captopril, enalapril, lisinopril, ramipril, and fosinopril. These medications are generally well-tolerated, but they can cause side effects such as cough, dizziness, headache, and elevated potassium levels in the blood. It is important for patients to follow their healthcare provider's instructions carefully when taking ACE inhibitors and to report any unusual symptoms or side effects promptly.

Interstitial nephritis is a condition characterized by inflammation in the interstitium (the tissue between the kidney tubules) of one or both kidneys. This inflammation can be caused by various factors, including infections, autoimmune disorders, medications, and exposure to certain toxins.

The inflammation may lead to symptoms such as hematuria (blood in the urine), proteinuria (protein in the urine), decreased urine output, and kidney dysfunction. In some cases, interstitial nephritis can progress to chronic kidney disease or even end-stage renal failure if left untreated.

The diagnosis of interstitial nephritis typically involves a combination of medical history, physical examination, laboratory tests (such as urinalysis and blood tests), and imaging studies (such as ultrasound or CT scan). A kidney biopsy may also be performed to confirm the diagnosis and assess the severity of the inflammation.

Treatment for interstitial nephritis depends on the underlying cause, but may include corticosteroids, immunosuppressive medications, or discontinuation of any offending medications. In some cases, supportive care such as dialysis may be necessary to manage kidney dysfunction until the inflammation resolves.

Kidney tubules are the structural and functional units of the kidney responsible for reabsorption, secretion, and excretion of various substances. They are part of the nephron, which is the basic unit of the kidney's filtration and reabsorption process.

There are three main types of kidney tubules:

1. Proximal tubule: This is the initial segment of the kidney tubule that receives the filtrate from the glomerulus. It is responsible for reabsorbing approximately 65% of the filtrate, including water, glucose, amino acids, and electrolytes.
2. Loop of Henle: This U-shaped segment of the tubule consists of a thin descending limb, a thin ascending limb, and a thick ascending limb. The loop of Henle helps to concentrate urine by creating an osmotic gradient that allows water to be reabsorbed in the collecting ducts.
3. Distal tubule: This is the final segment of the kidney tubule before it empties into the collecting duct. It is responsible for fine-tuning the concentration of electrolytes and pH balance in the urine by selectively reabsorbing or secreting substances such as sodium, potassium, chloride, and hydrogen ions.

Overall, kidney tubules play a critical role in maintaining fluid and electrolyte balance, regulating acid-base balance, and removing waste products from the body.

The Glomerular Basement Membrane (GBM) is a part of the filtration barrier in the nephron of the kidney. It is a thin, porous sheet of extracellular matrix that lies between the glomerular endothelial cells and the visceral epithelial cells (podocytes). The GBM plays a crucial role in the process of ultrafiltration, allowing the passage of water and small molecules while preventing the loss of larger proteins into the urine. It is composed mainly of type IV collagen, laminin, nidogen, and heparan sulfate proteoglycans. Certain kidney diseases, such as Goodpasture's disease and some forms of glomerulonephritis, can involve damage to the GBM.

Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:

1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.

Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.

Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.

The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.

In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

AIDS-associated nephropathy (AAN) is a kidney disorder that primarily affects individuals with advanced HIV infection. It is characterized by distinctive changes in the structure and function of the glomeruli, which are the tiny filtering units inside the kidneys.

The medical definition of AIDS-associated nephropathy is:

A renal disease associated with advanced HIV infection, characterized by focal segmental glomerulosclerosis (FSGS), collapsing variant or HIV-associated nephropathy (HIVAN) causing proteinuria, azotemia, and progressive decline in kidney function. The condition is more prevalent in certain racial/ethnic groups, such as African Americans, Hispanics, and Native Americans.

AAN is often considered a complication of advanced HIV disease and can lead to end-stage renal failure if not properly managed. Antiretroviral therapy (ART) has been shown to improve outcomes in patients with AAN, although some individuals may still require dialysis or kidney transplantation.

Renal hypertension, also known as renovascular hypertension, is a type of secondary hypertension (high blood pressure) that is caused by narrowing or obstruction of the renal arteries or veins, which supply blood to the kidneys. This can lead to decreased blood flow and oxygen delivery to the kidney tissue, activating the renin-angiotensin-aldosterone system (RAAS) and resulting in increased peripheral vascular resistance, sodium retention, and extracellular fluid volume, ultimately causing hypertension.

Renal hypertension can be classified into two types:

1. Renin-dependent renal hypertension: This is caused by a decrease in blood flow to the kidneys, leading to increased renin release from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that causes an increase in peripheral vascular resistance and blood pressure.
2. Renin-independent renal hypertension: This is caused by increased sodium retention and extracellular fluid volume, leading to an increase in blood pressure. This can be due to various factors such as obstructive sleep apnea, primary aldosteronism, or pheochromocytoma.

Renal hypertension is often asymptomatic but can lead to serious complications such as kidney damage, heart failure, and stroke if left untreated. Diagnosis of renal hypertension involves imaging studies such as renal artery duplex ultrasound, CT angiography, or magnetic resonance angiography (MRA) to identify any narrowing or obstruction in the renal arteries or veins. Treatment options include medications such as ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, and diuretics, as well as interventions such as angioplasty and stenting to improve blood flow to the kidneys.

Kidney transplantation is a surgical procedure where a healthy kidney from a deceased or living donor is implanted into a patient with end-stage renal disease (ESRD) or permanent kidney failure. The new kidney takes over the functions of filtering waste and excess fluids from the blood, producing urine, and maintaining the body's electrolyte balance.

The transplanted kidney is typically placed in the lower abdomen, with its blood vessels connected to the recipient's iliac artery and vein. The ureter of the new kidney is then attached to the recipient's bladder to ensure proper urine flow. Following the surgery, the patient will require lifelong immunosuppressive therapy to prevent rejection of the transplanted organ by their immune system.

Pre-eclampsia is a pregnancy-related disorder, typically characterized by the onset of high blood pressure (hypertension) and damage to organs, such as the kidneys, after the 20th week of pregnancy. It is often accompanied by proteinuria, which is the presence of excess protein in the urine. Pre-eclampsia can lead to serious complications for both the mother and the baby if left untreated or unmanaged.

The exact causes of pre-eclampsia are not fully understood, but it is believed that placental issues, genetic factors, and immune system problems may contribute to its development. Risk factors include first-time pregnancies, history of pre-eclampsia in previous pregnancies, chronic hypertension, obesity, older age (35 or older), and assisted reproductive technology (ART) pregnancies.

Pre-eclampsia can progress to a more severe form called eclampsia, which is characterized by the onset of seizures. HELLP syndrome, another severe complication, involves hemolysis (breaking down of red blood cells), elevated liver enzymes, and low platelet count.

Early detection and management of pre-eclampsia are crucial to prevent severe complications. Regular prenatal care, including frequent blood pressure checks and urine tests, can help identify early signs of the condition. Treatment typically involves close monitoring, medication to lower blood pressure, corticosteroids to promote fetal lung maturity, and, in some cases, delivery of the baby if the mother's or baby's health is at risk.

Immunosuppressive agents are medications that decrease the activity of the immune system. They are often used to prevent the rejection of transplanted organs and to treat autoimmune diseases, where the immune system mistakenly attacks the body's own tissues. These drugs work by interfering with the immune system's normal responses, which helps to reduce inflammation and damage to tissues. However, because they suppress the immune system, people who take immunosuppressive agents are at increased risk for infections and other complications. Examples of immunosuppressive agents include corticosteroids, azathioprine, cyclophosphamide, mycophenolate mofetil, tacrolimus, and sirolimus.

Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor, which is a type of medication used to treat various cardiovascular conditions. It works by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in relaxation and widening of blood vessels, decreased blood pressure, and increased blood flow.

Lisinopril is primarily used to treat hypertension (high blood pressure), congestive heart failure, and to improve survival after a heart attack. It may also be used to protect the kidneys from damage due to diabetes or high blood pressure. Additionally, it has been shown to reduce proteinuria (excess protein in urine) in patients with diabetic nephropathy.

Common side effects of Lisinopril include dizziness, headache, fatigue, and cough. More serious side effects may include angioedema (rapid swelling of the face, lips, tongue, or throat), hyperkalemia (elevated potassium levels), and impaired kidney function.

It is important to follow the prescribing physician's instructions carefully when taking Lisinopril and to report any unusual symptoms promptly. Regular monitoring of blood pressure, kidney function, and electrolyte levels may be necessary during treatment with this medication.

Angiotensin II Type 1 Receptor Blockers (ARBs) are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a hormone that causes blood vessels to constrict and blood pressure to increase, at its type 1 receptor. By blocking this effect, ARBs cause blood vessels to dilate, reducing blood pressure and decreasing the workload on the heart. Examples of ARBs include losartan, valsartan, irbesartan, and candesartan.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

The Glomerular Filtration Barrier is a complex structure in the kidney that is responsible for the initial filtration of blood in the nephron. It is made up of three layers: the fenestrated endothelial cells, the glomerular basement membrane (GBM), and the epithelial cells (podocytes) with their interdigitating foot processes. This barrier allows for the filtration of small molecules, such as water and solutes, while preventing the passage of larger molecules, like proteins, into the urinary space. The proper functioning of this barrier is crucial for maintaining normal kidney function and overall health.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

Chronic Renal Insufficiency (CRI) is a medical condition characterized by a gradual and progressive loss of kidney function over a period of months or years. It is also known as Chronic Kidney Disease (CKD). The main function of the kidneys is to filter waste products and excess fluids from the blood, which are then excreted in the urine. When the kidneys become insufficient, these waste products and fluids accumulate in the body, leading to various complications.

CRI is defined as a glomerular filtration rate (GFR) of less than 60 ml/min/1.73m2 for three months or more, regardless of cause. GFR is a measure of kidney function that estimates how well the kidneys are filtering waste products from the blood. The condition is classified into five stages based on the severity of the disease and the GFR value.

Stage 1: GFR greater than or equal to 90 ml/min/1.73m2
Stage 2: GFR between 60-89 ml/min/1.73m2
Stage 3: GFR between 30-59 ml/min/1.73m2
Stage 4: GFR between 15-29 ml/min/1.73m2
Stage 5: GFR less than 15 ml/min/1.73m2 or dialysis

CRI can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and other genetic or acquired disorders. Symptoms of CRI may include fatigue, weakness, loss of appetite, swelling in the legs and ankles, shortness of breath, and changes in urination patterns. Treatment for CRI focuses on slowing down the progression of the disease, managing symptoms, and preventing complications. This may involve lifestyle modifications, medication, dialysis, or kidney transplantation.

Reagent strips, also known as diagnostic or test strips, are narrow pieces of plastic material that have been impregnated with chemical reagents. They are used in the qualitative or semi-quantitative detection of various substances, such as glucose, proteins, ketones, blood, and white blood cells, in body fluids like urine or blood.

Reagent strips typically contain multiple pad areas, each with a different reagent that reacts to a specific substance. To perform the test, a small amount of the fluid is applied to the strip, and the reaction between the reagents and the target substance produces a visible color change. The resulting color can then be compared to a standardized color chart to determine the concentration or presence of the substance.

Reagent strips are widely used in point-of-care testing, providing quick and convenient results for healthcare professionals and patients alike. They are commonly used for monitoring conditions such as diabetes (urine or blood glucose levels), urinary tract infections (leukocytes and nitrites), and kidney function (protein and blood).

Renal insufficiency, also known as kidney failure, is a medical condition in which the kidneys are unable to properly filter waste products and excess fluids from the blood. This results in a buildup of these substances in the body, which can cause a variety of symptoms such as weakness, shortness of breath, and fluid retention. Renal insufficiency can be acute, meaning it comes on suddenly, or chronic, meaning it develops over time. It is typically diagnosed through blood tests, urine tests, and imaging studies. Treatment may include medications to control symptoms, dietary changes, and in severe cases, dialysis or a kidney transplant.

Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.

In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:

* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)

Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.

'NZB mice' is a term used to refer to an inbred strain of laboratory mice that are genetically identical to each other and have been used extensively in biomedical research. The 'NZB' designation stands for "New Zealand Black," which refers to the coat color of these mice.

NZB mice are known to spontaneously develop an autoimmune disease that is similar to human systemic lupus erythematosus (SLE), a chronic inflammatory disorder caused by an overactive immune system. This makes them a valuable model for studying the genetic and environmental factors that contribute to the development of SLE, as well as for testing new therapies and treatments.

It's important to note that while NZB mice are an inbred strain, they may still exhibit some variability in their disease phenotype due to genetic modifiers or environmental influences. Therefore, researchers often use large cohorts of mice and standardized experimental conditions to ensure the reproducibility and reliability of their findings.

Immune complex diseases are medical conditions that occur when the immune system produces an abnormal response to certain antigens, leading to the formation and deposition of immune complexes in various tissues and organs. These immune complexes consist of antibodies bound to antigens, which can trigger an inflammatory reaction and damage the surrounding tissue.

Immune complex diseases can be classified into two categories: acute and chronic. Acute immune complex diseases include serum sickness and hypersensitivity vasculitis, while chronic immune complex diseases include systemic lupus erythematosus (SLE), rheumatoid arthritis, and membranoproliferative glomerulonephritis.

The symptoms of immune complex diseases depend on the location and extent of tissue damage. They can range from mild to severe and may include fever, joint pain, skin rashes, kidney dysfunction, and neurological problems. Treatment typically involves medications that suppress the immune system and reduce inflammation, such as corticosteroids, immunosuppressants, and anti-inflammatory drugs.

The basement membrane is a thin, specialized layer of extracellular matrix that provides structural support and separates epithelial cells (which line the outer surfaces of organs and blood vessels) from connective tissue. It is composed of two main layers: the basal lamina, which is produced by the epithelial cells, and the reticular lamina, which is produced by the connective tissue. The basement membrane plays important roles in cell adhesion, migration, differentiation, and survival.

The basal lamina is composed mainly of type IV collagen, laminins, nidogens, and proteoglycans, while the reticular lamina contains type III collagen, fibronectin, and other matrix proteins. The basement membrane also contains a variety of growth factors and cytokines that can influence cell behavior.

Defects in the composition or organization of the basement membrane can lead to various diseases, including kidney disease, eye disease, and skin blistering disorders.

Antihypertensive agents are a class of medications used to treat high blood pressure (hypertension). They work by reducing the force and rate of heart contractions, dilating blood vessels, or altering neurohormonal activation to lower blood pressure. Examples include diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers, and direct vasodilators. These medications may be used alone or in combination to achieve optimal blood pressure control.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Enalapril is a medication that belongs to a class of drugs called angiotensin-converting enzyme (ACE) inhibitors. It works by blocking the action of a hormone in the body called angiotensin II, which causes blood vessels to narrow and tighten. By blocking this hormone, Enalapril helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the heart.

Enalapril is commonly used to treat high blood pressure (hypertension), congestive heart failure, and to improve survival after a heart attack. It may also be used to treat other conditions as determined by your doctor.

The medication comes in the form of tablets or capsules that are taken orally, usually once or twice a day with or without food. The dosage will depend on various factors such as the patient's age, weight, and medical condition. It is important to follow the instructions of your healthcare provider when taking Enalapril.

Like all medications, Enalapril can cause side effects, including dry cough, dizziness, headache, fatigue, and nausea. More serious side effects may include allergic reactions, kidney problems, and low blood pressure. If you experience any concerning symptoms while taking Enalapril, it is important to contact your healthcare provider right away.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

Medical Definition:

"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.

Hypoalbuminemia is a medical condition characterized by having lower than normal levels of albumin in the blood. Albumin is a type of protein produced by the liver, and it plays a crucial role in maintaining oncotic pressure (the force that keeps fluid inside blood vessels) and transporting various substances throughout the body.

A serum albumin level below 3.5 g/dL (grams per deciliter) is generally considered hypoalbuminemia, although some laboratories may define it as a level below 3.4 g/dL or even lower. This condition can be caused by various factors, including liver disease, malnutrition, kidney disease, inflammation, and protein-losing enteropathy (a disorder that causes excessive loss of protein in the gastrointestinal tract).

Hypoalbuminemia is often associated with poorer clinical outcomes in several medical conditions, such as increased risk of infection, longer hospital stays, and higher mortality rates. It's essential to identify and address the underlying cause of hypoalbuminemia for appropriate treatment and improved patient outcomes.

A chronic disease is a long-term medical condition that often progresses slowly over a period of years and requires ongoing management and care. These diseases are typically not fully curable, but symptoms can be managed to improve quality of life. Common chronic diseases include heart disease, stroke, cancer, diabetes, arthritis, and COPD (chronic obstructive pulmonary disease). They are often associated with advanced age, although they can also affect children and younger adults. Chronic diseases can have significant impacts on individuals' physical, emotional, and social well-being, as well as on healthcare systems and society at large.

Low-Density Lipoprotein Receptor-Related Protein 2 (LRP2), also known as Megalin, is a large transmembrane protein that belongs to the low-density lipoprotein receptor family. It is primarily expressed in the epithelial cells of various organs, including the kidneys, brain, and liver.

LRP2 plays a crucial role in endocytosis and intracellular signaling by binding to a wide range of ligands, such as lipoproteins, proteases, enzyme inhibitors, and vitamins. In the kidneys, LRP2 is involved in the reabsorption of filtered proteins and the clearance of circulating substances from the primary urine.

In the central nervous system, LRP2 is essential for the development and maintenance of the brain by mediating the uptake of various molecules necessary for neuronal survival and function. Mutations in the LRP2 gene have been associated with several genetic disorders, including Donnai-Barrow syndrome and facio-oculo-acoustico-renal (FOAR) syndrome, which are characterized by developmental abnormalities affecting multiple organ systems.

Mycophenolic Acid (MPA) is an immunosuppressive drug that is primarily used to prevent rejection in organ transplantation. It works by inhibiting the enzyme inosine monophosphate dehydrogenase, which is a key enzyme for the de novo synthesis of guanosine nucleotides, an essential component for the proliferation of T and B lymphocytes. By doing this, MPA reduces the activity of the immune system, thereby preventing it from attacking the transplanted organ.

Mycophenolic Acid is available in two forms: as the sodium salt (Mycophenolate Sodium) and as the morpholinoethyl ester (Mycophenolate Mofetil), which is rapidly hydrolyzed to Mycophenolic Acid after oral administration. Common side effects of MPA include gastrointestinal symptoms such as diarrhea, nausea, and vomiting, as well as an increased risk of infections due to its immunosuppressive effects.

Serum albumin is the most abundant protein in human blood plasma, synthesized by the liver. It plays a crucial role in maintaining the oncotic pressure or colloid osmotic pressure of blood, which helps to regulate the fluid balance between the intravascular and extravascular spaces.

Serum albumin has a molecular weight of around 66 kDa and is composed of a single polypeptide chain. It contains several binding sites for various endogenous and exogenous substances, such as bilirubin, fatty acids, hormones, and drugs, facilitating their transport throughout the body. Additionally, albumin possesses antioxidant properties, protecting against oxidative damage.

Albumin levels in the blood are often used as a clinical indicator of liver function, nutritional status, and overall health. Low serum albumin levels may suggest liver disease, malnutrition, inflammation, or kidney dysfunction.

Henoch-Schönlein purpura (HSP) is a type of small vessel vasculitis, which is a condition characterized by inflammation of the blood vessels. HSP primarily affects children, but it can occur in adults as well. It is named after two German physicians, Eduard Heinrich Henoch and Johann Schönlein, who first described the condition in the mid-19th century.

The main feature of HSP is a purpuric rash, which is a type of rash that appears as small, red or purple spots on the skin. The rash is caused by leakage of blood from the small blood vessels (capillaries) beneath the skin. In HSP, this rash typically occurs on the legs and buttocks, but it can also affect other parts of the body, such as the arms, face, and trunk.

In addition to the purpuric rash, HSP is often accompanied by other symptoms, such as joint pain and swelling, abdominal pain, nausea, vomiting, and diarrhea. In severe cases, it can also affect the kidneys, leading to hematuria (blood in the urine) and proteinuria (protein in the urine).

The exact cause of HSP is not known, but it is thought to be related to an abnormal immune response to certain triggers, such as infections or medications. Treatment typically involves supportive care, such as pain relief and fluid replacement, as well as medications to reduce inflammation and suppress the immune system. In most cases, HSP resolves on its own within a few weeks or months, but it can lead to serious complications in some individuals.

The Renin-Angiotensin System (RAS) is a complex hormonal system that regulates blood pressure, fluid and electrolyte balance, and vascular resistance. It plays a crucial role in the pathophysiology of hypertension, heart failure, and kidney diseases.

Here's a brief overview of how it works:

1. Renin is an enzyme that is released by the juxtaglomerular cells in the kidneys in response to decreased blood pressure or reduced salt delivery to the distal tubules.
2. Renin acts on a protein called angiotensinogen, which is produced by the liver, converting it into angiotensin I.
3. Angiotensin-converting enzyme (ACE), found in the lungs and other tissues, then converts angiotensin I into angiotensin II, a potent vasoconstrictor that narrows blood vessels and increases blood pressure.
4. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.
5. Additionally, angiotensin II has direct effects on the heart, promoting hypertrophy and remodeling, which can contribute to heart failure.
6. The RAS can be modulated by various medications, such as ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists, which are commonly used to treat hypertension, heart failure, and kidney diseases.

Losartan is an angiotensin II receptor blocker (ARB) medication that is primarily used to treat hypertension (high blood pressure), but can also be used to manage chronic heart failure and protect against kidney damage in patients with type 2 diabetes. It works by blocking the action of angiotensin II, a hormone that causes blood vessels to narrow and blood pressure to rise. By blocking this hormone's effects, losartan helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system.

The medical definition of losartan is: "A synthetic angiotensin II receptor antagonist used in the treatment of hypertension, chronic heart failure, and diabetic nephropathy. It selectively blocks the binding of angiotensin II to the AT1 receptor, leading to vasodilation, decreased aldosterone secretion, and increased renin activity."

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Bence Jones protein is a type of immunoglobulin light chain that can be detected in the urine or blood of some patients with certain diseases, most notably multiple myeloma. It's named after Henry Bence Jones, a 19th-century English physician who first described it.

These proteins are produced by malignant plasma cells, which are a type of white blood cell found in the bone marrow. In multiple myeloma, these cancerous cells multiply and produce abnormal amounts of immunoglobulins, leading to the overproduction of Bence Jones proteins.

When these proteins are excreted in the urine, they can cause damage to the kidneys, leading to kidney dysfunction or failure. Therefore, the detection of Bence Jones protein in the urine can be a sign of multiple myeloma or other related diseases. However, it's important to note that not all patients with multiple myeloma will have Bence Jones proteins in their urine.

Anti-glomerular basement membrane (anti-GBM) disease, also known as Goodpasture's disease, is a rare autoimmune disorder in which the body produces antibodies that attack the glomerular basement membrane (GBM), a component of the filtering units (glomeruli) in the kidneys. This leads to inflammation and damage to the glomeruli, causing hematuria (blood in urine), proteinuria (protein in urine), and potentially kidney failure. In some cases, anti-GBM disease may also affect the lungs, leading to coughing up blood (hemoptysis). The exact cause of anti-GBM disease is not fully understood, but it is believed to be related to both genetic and environmental factors. Treatment typically involves a combination of immunosuppressive therapy and plasma exchange.

Antinuclear antibodies (ANA) are a type of autoantibody that target structures found in the nucleus of a cell. These antibodies are produced by the immune system and attack the body's own cells and tissues, leading to inflammation and damage. The presence of ANA is often used as a marker for certain autoimmune diseases, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.

ANA can be detected through a blood test called the antinuclear antibody test. A positive result indicates the presence of ANA in the blood, but it does not necessarily mean that a person has an autoimmune disease. Further testing is usually needed to confirm a diagnosis and determine the specific type of autoantibodies present.

It's important to note that ANA can also be found in healthy individuals, particularly as they age. Therefore, the test results should be interpreted in conjunction with other clinical findings and symptoms.

Nephrosclerosis is a medical term that refers to the thickening and scarring (fibrosis) of the small arteries and arterioles in the kidneys, resulting in reduced blood flow and damage to the kidney tissue. This process can lead to decreased kidney function and ultimately result in chronic kidney disease or end-stage renal failure.

The two main types of nephrosclerosis are:

1. Hypertensive nephrosclerosis: This type is caused by long-term high blood pressure (hypertension), which damages the small blood vessels in the kidneys over time, leading to scarring and thickening of the arterial walls.
2. Ischemic nephrosclerosis: This type results from reduced blood flow to the kidneys due to atherosclerosis or other vascular diseases that cause narrowing or blockage of the renal arteries.

Nephrosclerosis is often asymptomatic in its early stages, but as the condition progresses, it may lead to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), and hypertension. Diagnosis typically involves a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment focuses on managing underlying conditions such as high blood pressure and diabetes, which can help slow or prevent further kidney damage.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Tetrazoles are a class of heterocyclic aromatic organic compounds that contain a five-membered ring with four nitrogen atoms and one carbon atom. They have the chemical formula of C2H2N4. Tetrazoles are stable under normal conditions, but can decompose explosively when heated or subjected to strong shock.

In the context of medicinal chemistry, tetrazoles are sometimes used as bioisosteres for carboxylic acids, as they can mimic some of their chemical and biological properties. This has led to the development of several drugs that contain tetrazole rings, such as the antiviral drug tenofovir and the anti-inflammatory drug celecoxib.

However, it's important to note that 'tetrazoles' is not a medical term per se, but rather a chemical term that can be used in the context of medicinal chemistry or pharmacology.

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease that can affect almost any organ or system in the body. In SLE, the immune system produces an exaggerated response, leading to the production of autoantibodies that attack the body's own cells and tissues, causing inflammation and damage. The symptoms and severity of SLE can vary widely from person to person, but common features include fatigue, joint pain, skin rashes (particularly a "butterfly" rash across the nose and cheeks), fever, hair loss, and sensitivity to sunlight.

Systemic lupus erythematosus can also affect the kidneys, heart, lungs, brain, blood vessels, and other organs, leading to a wide range of symptoms such as kidney dysfunction, chest pain, shortness of breath, seizures, and anemia. The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. Treatment typically involves medications to suppress the immune system and manage symptoms, and may require long-term management by a team of healthcare professionals.

Combination drug therapy is a treatment approach that involves the use of multiple medications with different mechanisms of action to achieve better therapeutic outcomes. This approach is often used in the management of complex medical conditions such as cancer, HIV/AIDS, and cardiovascular diseases. The goal of combination drug therapy is to improve efficacy, reduce the risk of drug resistance, decrease the likelihood of adverse effects, and enhance the overall quality of life for patients.

In combining drugs, healthcare providers aim to target various pathways involved in the disease process, which may help to:

1. Increase the effectiveness of treatment by attacking the disease from multiple angles.
2. Decrease the dosage of individual medications, reducing the risk and severity of side effects.
3. Slow down or prevent the development of drug resistance, a common problem in chronic diseases like HIV/AIDS and cancer.
4. Improve patient compliance by simplifying dosing schedules and reducing pill burden.

Examples of combination drug therapy include:

1. Antiretroviral therapy (ART) for HIV treatment, which typically involves three or more drugs from different classes to suppress viral replication and prevent the development of drug resistance.
2. Chemotherapy regimens for cancer treatment, where multiple cytotoxic agents are used to target various stages of the cell cycle and reduce the likelihood of tumor cells developing resistance.
3. Cardiovascular disease management, which may involve combining medications such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, and statins to control blood pressure, heart rate, fluid balance, and cholesterol levels.
4. Treatment of tuberculosis, which often involves a combination of several antibiotics to target different aspects of the bacterial life cycle and prevent the development of drug-resistant strains.

When prescribing combination drug therapy, healthcare providers must carefully consider factors such as potential drug interactions, dosing schedules, adverse effects, and contraindications to ensure safe and effective treatment. Regular monitoring of patients is essential to assess treatment response, manage side effects, and adjust the treatment plan as needed.

Serum sickness is an immune-mediated hypersensitivity reaction that typically occurs within 1 to 3 weeks after the administration of foreign proteins or drugs, such as certain types of antibiotics, antiserums, or monoclonal antibodies. It is characterized by symptoms such as fever, rash, joint pain, and lymphadenopathy (swollen lymph nodes). These symptoms are caused by the formation of immune complexes, which deposit in various tissues and activate the complement system, leading to inflammation. Serum sickness can be treated with antihistamines, corticosteroids, and other immunomodulatory agents. It is important to note that serum sickness is different from anaphylaxis, which is a more severe, life-threatening allergic reaction that occurs immediately after exposure to an allergen.

Complement C3 is a protein that plays a central role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3 can be activated through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Once activated, it breaks down into two fragments, C3a and C3b.

C3a is an anaphylatoxin that helps to recruit immune cells to the site of infection or injury, while C3b plays a role in opsonization, which is the process of coating pathogens or damaged cells with proteins to make them more recognizable to the immune system. Additionally, C3b can also activate the membrane attack complex (MAC), which forms a pore in the membrane of target cells leading to their lysis or destruction.

In summary, Complement C3 is an important protein in the complement system that helps to identify and eliminate pathogens and damaged cells from the body through various mechanisms.

The glomerular mesangium is a part of the nephron in the kidney. It is the region located in the middle of the glomerular tuft, where the capillary loops of the glomerulus are surrounded by a network of extracellular matrix and mesangial cells. These cells and matrix play an important role in maintaining the structure and function of the filtration barrier in the glomerulus, which helps to filter waste products from the blood.

The mesangial cells have contractile properties and can regulate the flow of blood through the capillaries by constricting or dilating the diameter of the glomerular capillary loops. They also play a role in immune responses, as they can phagocytize immune complexes and release cytokines and growth factors that modulate inflammation and tissue repair.

Abnormalities in the mesangium can lead to various kidney diseases, such as glomerulonephritis, mesangial proliferative glomerulonephritis, and diabetic nephropathy.

The Complement Membrane Attack Complex (MAC), also known as the Terminal Complement Complex (TCC), is a protein structure that forms in the final stages of the complement system's immune response. The complement system is a part of the innate immune system that helps to eliminate pathogens and damaged cells from the body.

The MAC is composed of several proteins, including C5b, C6, C7, C8, and multiple subunits of C9, which assemble on the surface of target cells. The formation of the MAC creates a pore-like structure in the cell membrane, leading to disruption of the membrane's integrity and ultimately causing cell lysis or damage.

The MAC plays an important role in the immune response by helping to eliminate pathogens that have evaded other immune defenses. However, uncontrolled activation of the complement system and formation of the MAC can also contribute to tissue damage and inflammation in various diseases, such as autoimmune disorders, age-related macular degeneration, and ischemia-reperfusion injury.

Follow-up studies are a type of longitudinal research that involve repeated observations or measurements of the same variables over a period of time, in order to understand their long-term effects or outcomes. In medical context, follow-up studies are often used to evaluate the safety and efficacy of medical treatments, interventions, or procedures.

In a typical follow-up study, a group of individuals (called a cohort) who have received a particular treatment or intervention are identified and then followed over time through periodic assessments or data collection. The data collected may include information on clinical outcomes, adverse events, changes in symptoms or functional status, and other relevant measures.

The results of follow-up studies can provide important insights into the long-term benefits and risks of medical interventions, as well as help to identify factors that may influence treatment effectiveness or patient outcomes. However, it is important to note that follow-up studies can be subject to various biases and limitations, such as loss to follow-up, recall bias, and changes in clinical practice over time, which must be carefully considered when interpreting the results.

Amyloidosis is a medical condition characterized by the abnormal accumulation of insoluble proteins called amyloid in various tissues and organs throughout the body. These misfolded protein deposits can disrupt the normal function of affected organs, leading to a range of symptoms depending on the location and extent of the amyloid deposition.

There are different types of amyloidosis, classified based on the specific proteins involved:

1. Primary (AL) Amyloidosis: This is the most common form, accounting for around 80% of cases. It results from the overproduction and misfolding of immunoglobulin light chains, typically by clonal plasma cells in the bone marrow. The amyloid deposits can affect various organs, including the heart, kidneys, liver, and nervous system.
2. Secondary (AA) Amyloidosis: This form is associated with chronic inflammatory diseases, such as rheumatoid arthritis, tuberculosis, or familial Mediterranean fever. The amyloid fibrils are composed of serum amyloid A protein (SAA), an acute-phase reactant produced during the inflammatory response. The kidneys are commonly affected in this type of amyloidosis.
3. Hereditary or Familial Amyloidosis: These forms are caused by genetic mutations that result in the production of abnormal proteins prone to misfolding and amyloid formation. Examples include transthyretin (TTR) amyloidosis, fibrinogen amyloidosis, and apolipoprotein AI amyloidosis. These forms can affect various organs, including the heart, nerves, and kidneys.
4. Dialysis-Related Amyloidosis: This form is seen in patients undergoing long-term dialysis for chronic kidney disease. The amyloid fibrils are composed of beta-2 microglobulin, a protein that accumulates due to impaired clearance during dialysis. The joints and bones are commonly affected in this type of amyloidosis.

The diagnosis of amyloidosis typically involves a combination of clinical evaluation, imaging studies, and tissue biopsy with the demonstration of amyloid deposition using special stains (e.g., Congo red). Treatment depends on the specific type and extent of organ involvement and may include supportive care, medications to target the underlying cause (e.g., chemotherapy, immunomodulatory agents), and organ transplantation in some cases.

Diabetes Mellitus, Type 2 is a metabolic disorder characterized by high blood glucose (or sugar) levels resulting from the body's inability to produce sufficient amounts of insulin or effectively use the insulin it produces. This form of diabetes usually develops gradually over several years and is often associated with older age, obesity, physical inactivity, family history of diabetes, and certain ethnicities.

In Type 2 diabetes, the body's cells become resistant to insulin, meaning they don't respond properly to the hormone. As a result, the pancreas produces more insulin to help glucose enter the cells. Over time, the pancreas can't keep up with the increased demand, leading to high blood glucose levels and diabetes.

Type 2 diabetes is managed through lifestyle modifications such as weight loss, regular exercise, and a healthy diet. Medications, including insulin therapy, may also be necessary to control blood glucose levels and prevent long-term complications associated with the disease, such as heart disease, nerve damage, kidney damage, and vision loss.

The proximal kidney tubule is the initial portion of the renal tubule in the nephron of the kidney. It is located in the renal cortex and is called "proximal" because it is closer to the glomerulus, compared to the distal tubule. The proximal tubule plays a crucial role in the reabsorption of water, electrolytes, and nutrients from the filtrate that has been formed by the glomerulus. It also helps in the secretion of waste products and other substances into the urine.

The proximal tubule is divided into two segments: the pars convoluta and the pars recta. The pars convoluta is the curved portion that receives filtrate from the Bowman's capsule, while the pars recta is the straight portion that extends deeper into the renal cortex.

The proximal tubule is lined with a simple cuboidal epithelium, and its cells are characterized by numerous mitochondria, which provide energy for active transport processes. The apical surface of the proximal tubular cells has numerous microvilli, forming a brush border that increases the surface area for reabsorption.

In summary, the proximal kidney tubule is a critical site for the reabsorption of water, electrolytes, and nutrients from the glomerular filtrate, contributing to the maintenance of fluid and electrolyte balance in the body.

Fibrosis is a pathological process characterized by the excessive accumulation and/or altered deposition of extracellular matrix components, particularly collagen, in various tissues and organs. This results in the formation of fibrous scar tissue that can impair organ function and structure. Fibrosis can occur as a result of chronic inflammation, tissue injury, or abnormal repair mechanisms, and it is a common feature of many diseases, including liver cirrhosis, lung fibrosis, heart failure, and kidney disease.

In medical terms, fibrosis is defined as:

"The process of producing scar tissue (consisting of collagen) in response to injury or chronic inflammation in normal connective tissue. This can lead to the thickening and stiffening of affected tissues and organs, impairing their function."

Prednisolone is a synthetic glucocorticoid drug, which is a class of steroid hormones. It is commonly used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects. Prednisolone works by binding to specific receptors in cells, leading to changes in gene expression that reduce the production of substances involved in inflammation, such as cytokines and prostaglandins.

Prednisolone is available in various forms, including tablets, syrups, and injectable solutions. It can be used to treat a wide range of medical conditions, including asthma, rheumatoid arthritis, inflammatory bowel disease, allergies, skin conditions, and certain types of cancer.

Like other steroid medications, prednisolone can have significant side effects if used in high doses or for long periods of time. These may include weight gain, mood changes, increased risk of infections, osteoporosis, diabetes, and adrenal suppression. As a result, the use of prednisolone should be closely monitored by a healthcare professional to ensure that its benefits outweigh its risks.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Nephrology is a branch of medicine that deals with the study and treatment of kidney diseases. A nephrologist is a medical specialist who specializes in the diagnosis, management, and treatment of various kidney-related disorders such as chronic kidney disease (CKD), acute renal failure, glomerulonephritis, hypertension, kidney stones, electrolyte imbalances, and inherited kidney diseases. They also provide care for patients who require dialysis or transplantation due to end-stage renal disease (ESRD). Nephrologists work closely with other healthcare professionals including primary care physicians, surgeons, radiologists, and pathologists to develop individualized treatment plans for their patients.

Pregnancy-induced hypertension (PIH), also known as gestational hypertension, is a condition characterized by the new onset of high blood pressure (≥140 mm Hg systolic or ≥90 mm Hg diastolic) after 20 weeks of pregnancy in a woman who was normotensive before. It can sometimes progress to more severe conditions like preeclampsia and eclampsia, which are associated with damage to other organ systems such as the liver and kidneys.

PIH is typically classified into two types:

1. Gestational hypertension: This is when a woman develops high blood pressure after 20 weeks of pregnancy without any protein in the urine or evidence of damage to other organ systems. Women with gestational hypertension are at increased risk for preeclampsia and may require closer monitoring.

2. Preeclampsia: This is a more severe form of PIH, characterized by high blood pressure and proteinuria (≥0.3 g in a 24-hour urine collection) after 20 weeks of pregnancy. Preeclampsia can also involve damage to other organ systems, such as the liver, kidneys, or brain, and may progress to eclampsia, a life-threatening condition characterized by seizures.

The exact causes of PIH are not fully understood, but it is thought to be related to problems with the development and function of the blood vessels that supply the placenta. Risk factors for developing PIH include first-time pregnancies, obesity, older age, a history of chronic hypertension or kidney disease, and carrying multiples (twins, triplets, etc.).

Treatment for PIH depends on the severity of the condition and the gestational age of the pregnancy. In mild cases, close monitoring of blood pressure, urine protein levels, and fetal growth may be sufficient. More severe cases may require medication to lower blood pressure, corticosteroids to promote fetal lung maturity, or early delivery of the baby to prevent further complications.

Retrospective studies, also known as retrospective research or looking back studies, are a type of observational study that examines data from the past to draw conclusions about possible causal relationships between risk factors and outcomes. In these studies, researchers analyze existing records, medical charts, or previously collected data to test a hypothesis or answer a specific research question.

Retrospective studies can be useful for generating hypotheses and identifying trends, but they have limitations compared to prospective studies, which follow participants forward in time from exposure to outcome. Retrospective studies are subject to biases such as recall bias, selection bias, and information bias, which can affect the validity of the results. Therefore, retrospective studies should be interpreted with caution and used primarily to generate hypotheses for further testing in prospective studies.

Ramipril is an angiotensin-converting enzyme (ACE) inhibitor, which is a type of medication used to treat various cardiovascular conditions. It works by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, thereby causing relaxation and widening of blood vessels, decreasing blood pressure, and increasing blood flow.

Ramipril is primarily used for the treatment of hypertension (high blood pressure), heart failure, and the prevention of major cardiovascular events such as myocardial infarction (heart attack) and stroke in high-risk patients. It may also be used to improve survival after a heart attack.

The medication is available in oral tablet form and is typically taken once or twice daily, depending on the prescribed dosage. Side effects of ramipril can include cough, dizziness, headache, fatigue, nausea, and taste changes. Serious side effects are rare but may include kidney problems, hyperkalemia (high potassium levels), and angioedema (swelling of the face, lips, tongue, or throat).

It is important to follow the prescribing physician's instructions carefully when taking ramipril and to report any unusual symptoms or side effects promptly. Regular monitoring of blood pressure, kidney function, and potassium levels may be necessary during treatment with this medication.

Transgenic rats are genetically modified rats that have incorporated foreign DNA (transgene) into their own genome. This is typically done through the use of recombinant DNA techniques in the laboratory. The transgene can come from any species, including other mammals, plants, or even bacteria. Once the transgene is introduced into the rat's embryonic cells, it becomes a permanent part of the rat's genetic makeup and is passed on to its offspring.

Transgenic rats are used in biomedical research as models for studying human diseases, developing new therapies, and testing the safety and efficacy of drugs. They offer several advantages over traditional laboratory rats, including the ability to manipulate specific genes, study gene function and regulation, and investigate the underlying mechanisms of disease.

Some common applications of transgenic rats in research include:

1. Modeling human diseases: Transgenic rats can be engineered to develop symptoms and characteristics of human diseases, such as cancer, diabetes, Alzheimer's, and Parkinson's. This allows researchers to study the disease progression, test new treatments, and evaluate their effectiveness.
2. Gene function and regulation: By introducing specific genes into rats, scientists can investigate their role in various biological processes, such as development, aging, and metabolism. They can also study how genes are regulated and how they interact with each other.
3. Drug development and testing: Transgenic rats can be used to test the safety and efficacy of new drugs before they are tested in humans. By studying the effects of drugs on transgenic rats, researchers can gain insights into their potential benefits and risks.
4. Toxicology studies: Transgenic rats can be used to study the toxicity of chemicals, pollutants, and other substances. This helps ensure that new products and treatments are safe for human use.

In summary, transgenic rats are genetically modified rats that have incorporated foreign DNA into their own genome. They are widely used in biomedical research to model human diseases, study gene function and regulation, develop new therapies, and test the safety and efficacy of drugs.

Alpha-globulins are a group of proteins present in blood plasma, which are classified based on their electrophoretic mobility. They migrate between albumin and beta-globulins during electrophoresis. Alpha-globulins include several proteins, such as alpha-1 antitrypsin, alpha-1 acid glycoprotein, and haptoglobin. These proteins play various roles in the body, including transporting and regulating other molecules, participating in immune responses, and maintaining oncotic pressure in blood vessels.

A Severity of Illness Index is a measurement tool used in healthcare to assess the severity of a patient's condition and the risk of mortality or other adverse outcomes. These indices typically take into account various physiological and clinical variables, such as vital signs, laboratory values, and co-morbidities, to generate a score that reflects the patient's overall illness severity.

Examples of Severity of Illness Indices include the Acute Physiology and Chronic Health Evaluation (APACHE) system, the Simplified Acute Physiology Score (SAPS), and the Mortality Probability Model (MPM). These indices are often used in critical care settings to guide clinical decision-making, inform prognosis, and compare outcomes across different patient populations.

It is important to note that while these indices can provide valuable information about a patient's condition, they should not be used as the sole basis for clinical decision-making. Rather, they should be considered in conjunction with other factors, such as the patient's overall clinical presentation, treatment preferences, and goals of care.

I'm happy to help! "Rats, Inbred Lew" is a specific strain of laboratory rats that have been inbred for research purposes. The "Lew" part of the name refers to the location where they were first developed, the Lewis Institute in Lake Bluff, Illinois, USA.

Inbreeding is a process of mating closely related individuals over many generations to create a genetically homogeneous population. This results in a high degree of genetic similarity among members of the strain, making them ideal for use as experimental models because any differences observed between individuals are more likely to be due to the experimental manipulation rather than genetic variation.

Inbred Lew rats have been widely used in biomedical research, particularly in studies related to hypertension and cardiovascular disease. They exhibit a number of unique characteristics that make them useful for these types of studies, including their susceptibility to developing high blood pressure when fed a high-salt diet or given certain drugs.

It's important to note that while inbred strains like Lew rats can be very useful tools for researchers, they are not perfect models for human disease. Because they have been bred in a controlled environment and selected for specific traits, they may not respond to experimental manipulations in the same way that humans or other animals would. Therefore, it's important to interpret findings from these studies with caution and consider multiple lines of evidence before drawing any firm conclusions.

Hereditary nephritis is a genetic disorder that causes recurring inflammation of the kidneys' glomeruli, which are the tiny blood vessel clusters that filter waste from the blood. This condition is also known as hereditary glomerulonephritis.

The inherited form of nephritis is caused by mutations in specific genes, leading to abnormalities in the proteins responsible for maintaining the structural integrity and proper functioning of the glomeruli. As a result, affected individuals typically experience hematuria (blood in urine), proteinuria (protein in urine), hypertension (high blood pressure), and progressive kidney dysfunction that can ultimately lead to end-stage renal disease (ESRD).

There are different types of hereditary nephritis, such as Alport syndrome and thin basement membrane nephropathy. These conditions have distinct genetic causes, clinical presentations, and inheritance patterns. Early diagnosis and appropriate management can help slow the progression of kidney damage and improve long-term outcomes for affected individuals.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Plasmapheresis is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies or toxins, is then removed and replaced with fresh plasma or a plasma substitute. The remaining blood cells are mixed with the new plasma and returned to the body. This process is also known as therapeutic plasma exchange (TPE). It's used to treat various medical conditions including certain autoimmune diseases, poisonings, and neurological disorders.

Cyclosporine is a medication that belongs to a class of drugs called immunosuppressants. It is primarily used to prevent the rejection of transplanted organs, such as kidneys, livers, and hearts. Cyclosporine works by suppressing the activity of the immune system, which helps to reduce the risk of the body attacking the transplanted organ.

In addition to its use in organ transplantation, cyclosporine may also be used to treat certain autoimmune diseases, such as rheumatoid arthritis and psoriasis. It does this by suppressing the overactive immune response that contributes to these conditions.

Cyclosporine is available in capsule, oral solution, and injectable forms. Common side effects of the medication include kidney problems, high blood pressure, tremors, headache, and nausea. Long-term use of cyclosporine can also increase the risk of certain types of cancer and infections.

It is important to note that cyclosporine should only be used under the close supervision of a healthcare provider, as it requires regular monitoring of blood levels and kidney function.

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Proteinuria. September 9, 7 am: Tired and exhausted. Weakness of all four extremities. Low morale. Body temperature 37 degrees ...
"Proteinuria". www.niddk.nih.gov. Retrieved 2015-06-14. Thomas, Donald E. Jr (2014-05-22). The Lupus Encyclopedia: A ... This condition is called proteinuria. Loss of necessary protein due to nephritis can result in several life-threatening ...
... proteinuria; and strontium. Rollo published Observations on the Diseases in the Army on St. Lucia, in 1781; and in 1785 Remarks ...
"Proteinuria". UK Renal Association. December 15, 2005. Archived from the original on August 14, 2007. clinlabnavigator.com > ... 2000). "The non-insulin-dependent diabetes, hypertension, microalbuminuria or proteinuria, cardiovascular events, and ramipril ...
Hebert LA, Charleston J, Miller E (2009). "Proteinuria". Archived from the original on 2011-05-05. Retrieved 2011-03-24. ...
... proteinuria, and/or wheezing; or very rarely, symptoms of overt anaphylaxis such as hives, angioedema (i.e. skin swelling in ... and proteinuria. The individuals exhibit greatly increased numbers off circulating NK cells, increased levels of T helper cells ...
... and proteinuria. Taking oral cetirizine regularly has been known to help those who suffer from skeeter syndrome.[citation ...
... and proteinuria. Affected individuals have increased blood levels of immunoglobulin E (which plays an essential role in the ...
Towards the end of his life Addis began to study laboratory rats as a model of proteinuria, and was among the first people to ... Addis T. (1932). "Proteinuria and cylinduria". Proceedings of the California Academy of Sciences. 2: 38-52. Schmitt, Ronald et ...
Orthostatic proteinuria (synonyms: orthostatic albuminuria, postural proteinuria) is a benign condition. A change in renal ... Ganong's review of medical physiology, 24th Edition "Orthostatic Proteinuria. What is Proteinuria? Causes, info". patient.info ... The exact cause for orthostatic proteinuria is not known. ...
Laboratory abnormalities include normal or mild decreases in serum C3, C4, and CH50 levels, and mild proteinuria. In contrast ... and mild proteinuria. Case reports have noted the absence of fever in serum sickness-like reactions to amoxicillin. ... proteinuria, and significant decreases in serum complement levels; it was originally described after patients were infused with ...
Addis T (1932). "Proteinuria and cylinduria". Proceedings of the California Academy of Sciences. 2: 38-52. Bell ME (September ... Urinary proteins were first reported in rodents in 1932, during studies by Thomas Addis into the cause of proteinuria. They are ... Therefore, since 1827 physicians and scientists have been interested in proteinuria, the excess of protein in human urine, as ... To better understand the etiology of proteinuria, some scientists attempted to study the phenomenon in laboratory animals. ...
Proteinuria, usually less than 2 grams per day, also may be present. Other renal causes of isolated hematuria include thin ... Proteinuria and hypertension are the most powerful prognostic factors in this group. There are certain other features on kidney ... Male sex, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidemia, older age, familial disease and elevated ... However, patients with isolated microscopic hematuria (i.e. without associated proteinuria and with normal kidney function) are ...
Ahuja TS (August 2003). "Doxycycline decreases proteinuria in glomerulonephritis". Am J Kidney Dis. 42 (2): 376-80. doi:10.1016 ...
... low molecular weight proteinuria; XD: X-linked dominant; XR: X-linked recessive; PTH: Parathyroid hormone "tubulopathy" at ...
While most women with HELLP syndrome have high blood pressure and proteinuria, up to 20% of HELLP syndrome cases do not present ... This diagnosis can be made even if the patient does not have proteinuria. Women with preeclampsia with severe features are ... Key signs are increased blood pressure and protein in the urine (proteinuria). Other symptoms that seem to occur with ... and proteinuria. Preeclampsia is a leading cause of fetal complications, which include low birth weight, preterm birth, and ...
A proteinuria of greater than 3.5 g /24 h /1.73 m2 (between 3 and 3.5 g/24 h /1.73 m2 is considered to be proteinuria in the ... Proteinuria: the loss of proteins from the urine is caused by many pathological agents and infection by these agents has to be ... "Relación de la proteinuria con el nivel de hemoglobina glicosilada en los diabéticos". Archived from the original on 2008-09-14 ... The urine sample is tested for proteinuria (>3.5 g per 1.73 m2 per 24 hours). It is also examined for urinary casts, which are ...
ISBN 978-0-8138-1844-3. Hasan, Shadi; Hassan, Kamal (2004-12-15). "Proteinuria associated with centipede bite". Pediatric ...
Proteinuria and hematuria are usually absent. Polyuria is resistant to vasopressin. When other organ systems are affected, ...
Microscopic haematuria with or without proteinuria may be seen in Class II Lupus nephritis. Hypertension, nephrotic syndrome, ... Presentation can also include asymptomatic proteinuria. These presenting symptoms are relatively non-specific and are often ... Preceding infection was not as readily identified in patients presenting with either asymptomatic proteinuria or nephrotic ...
Also a urine dipstick test for proteinuria can give a rough estimate of albuminuria. This is because albumin is by far the ... It is a type of proteinuria. Albumin is a major plasma protein (normally circulating in the blood); in healthy people, only ... For a number of reasons, clinical terminology is changing to focus on albuminuria more than proteinuria. It is usually ...
August 2010). "Melanocortin 1 receptor agonists reduce proteinuria". Journal of the American Society of Nephrology. 21 (8): ... it was found that treatment with a different agonist of MC1R improved aspects of kidney morphology and reduced proteinuria, ...
Urinalysis typically demonstrates hematuria and proteinuria. Levels of the complement protein C3 are low, while levels of C- ...
In kidney disease and nephrotic syndrome, albumin infusions as replacement for albumin loss to proteinuria is used in some ... Cil, Onur; Perwad, Farzana (2018). "Monogenic Causes of Proteinuria in Children". Frontiers in Medicine. 5: 55. doi:10.3389/ ... a CMP may be ordered as a follow-up test when proteinuria is detected by urine dipstick analysis, which may lead to a diagnosis ...
Sarafidis PA, Khosla N, Bakris GL (January 2007). "Antihypertensive therapy in the presence of proteinuria". American Journal ... as reducing glomerular filtration rate associated with a rise of serum creatinine in patients with pre-existing proteinuria, ...
Proteinuria, leucocytosis and elevated uric acid concentrations > 7.8 mg. Decreased serum haptoglobin and haemoglobin levels. ...
MAD1L1 Proteinuria, low molecular weight, with hypercalciuric nephrocalcinosis; 308990; CLCN5 Protoporphyria, erythropoietic, ...
... proteinuria, hematuria (blood in the urine), bladder injury; in animals: teratogenic effects. The short-term NOAEL of 9.6 - 10 ...
The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying ... Severe proteinuria can cause nephrotic syndrome in which there is worsening swelling of the body. Proteinuria often causes no ... overflow proteinuria) Due to low reabsorption at proximal tubule (Fanconi syndrome) Proteinuria can also be caused by certain ... diabetic proteinuria versus the field.[citation needed] With severe proteinuria, general hypoproteinemia can develop which ...
Orthostatic proteinuria is diagnosed if the patient has no proteinuria in early morning samples but has low-grade proteinuria ... Isolated, post-renal, and post-transplant proteinuria also deserve mention. Isolated proteinuria is proteinuria without any ... Tubular proteinuria. Tubular proteinuria is a result of tubulointersitial disease affecting the proximal renal tubules and ... Overflow proteinuria. Overflow proteinuria is most commonly associated with increased production of abnormal low molecular ...
Proteinuria in Pre and Post Transplant Patients with focal segmental glomerulosclerosis (FSGS) who progress rapidly to end ... proteinuria Clinical Research Trial Listings on CenterWatch ...
... who were included in the clinical trials of auranofin in the United States were examined for data on development of proteinuria ... proteinuria. Permanent renal impairment did not occur, and proteinuria did not persist beyond 12 months in most patients. Seven ... Proteinuria in gold-treated rheumatoid arthritis Ann Intern Med. 1984 Aug;101(2):176-9. doi: 10.7326/0003-4819-101-2-176. ... In similar groups of patients, the risk of developing proteinuria with auranofin therapy is significantly less than that with ...
... N Engl J Med. 1983 Dec 22;309(25):1543-6. doi: 10.1056/ ... can replace the 24-hour urine collection in the clinical quantitation of proteinuria. In the presence of stable renal function ... a protein/creatinine ratio of more than 3.5 (mg/mg) can be taken to represent "nephrotic-range" proteinuria, and a ratio of ...
Our 7 faculties and 12 professional schools offer more than 200 programmes to some 18,000 graduate, undergraduate and continuing studies students.. The UWI, Mona ranks first in Jamaica among accredited tertiary-level programmes. In 2012, the University was again one of Jamaicas Top 100 Employers.. ...
This reduction was associated with the disappearance of trace proteinuria from the technicians urine. Contamination of ...
i,Objective,/i,. To investigate association between maternofoetal complications and the amount of proteinuria measured by spot ... P. Chan, M. Brown, J. M. Simpson, and G. Davis, "Proteinuria in pre-eclampsia: how much matters?" An International Journal of ... However, proteinuria estimation seems to be promising as a candidate biomarker in predicting maternal and foetal outcome in ... Table 3 shows the outcome of labour in patients of preeclampsia and its association with the amount of proteinuria. 21% of the ...
In the cat, a UPC ratio ,0.4-0.5 is accepted as abnormal proteinuria. Proteinuria has been shown to occur in cats with immune- ... In this study, proteinuria was assessed in 100 randomly selected sick cats and 22 healthy cats by means of the urine protein: ... Proteinuria was significantly (P,0.014) more prevalent in the sick than the healthy cats with 36% and 9% respectively having ... Proteinuria may be measured quantitatively over 24 hours, or more simply by a random urine protein to creatinine (UPC) ratio ( ...
What are the causes and symptoms of Proteinuria - Protein is a standout amongst the most vital parts of the human body. Truth ... Symptoms Of Proteinuria. Proteinuria is a chronic ailment and once in a while does it demonstrate any manifestations amid the ... What are the causes and symptoms of Proteinuria?. HealthMedical Conditions & TreatmentMedical Research & StudiesGeneral Topics ... A few people are viewed as more in danger for proteinuria than others. For instance, African Americans are viewed as higher ...
M R Hussein, H I Hassan, E R M Hofny, M Elkholy, N A Fatehy, A E A Abd Elmoniem, A M Ezz El-Din, O A Afifi, H G Rashed ...
Hantavirus Infection with Renal Failure and Proteinuria, Colorado, USA, 2019 Swati Chand1, Sangharsha Thapa1, Shelley Kon, ... Hantavirus Infection with Renal Failure and Proteinuria, Colorado, USA, 2019. ...
placebo in proteinuria reduction at 36-week interim analysis1; the safety profile of atrasentan was consistent with previously ... Impact of Proteinuria and Kidney Function Decline on Health Care Costs and Resource Utilization in Adults With IgA Nephropathy ... Remission of Proteinuria Improves Prognosis in IgA Nephropathy. J Am Soc Nephrol. 2007;18(12):3177-3183. doi:10.1681/ASN. ... Up to 30% of people who have IgAN with persistent higher levels of proteinuria (≥1 g/day) progress to kidney failure within 10 ...
The degree of residual proteinuria is proportionally associated with renal risk as that of baseline proteinuria [16]. The ... It is not entirely clear how amiloride and triamterene attenuate proteinuria. In the process of proteinuria formation, a ... the role of uPAR in podocyte injury and proteinuria is controversial [10]. The effect of amiloride in reducing proteinuria in ... Proteinuria is an indicator of injury to the glomerular filtration barrier and has been a therapeutic target to manage CKD. ...
A 65-year-old man with hypertension for more than 30 years presents for evaluation of proteinuria. His hypertension has become ... Around 6 years ago, his estimated glomerular filtration rate (eGFR) was 50 mL/min/1.73 m2 with 6 g for proteinuria when ... A 65-Year-Old Man With Hypertension and Proteinuria - Medscape - Oct 12, 2015. ... black male with a history of hypertension for more than 30 years was referred to the nephrologist for evaluation of proteinuria ...
Explore fetal prognosis based on uricemia and maternal proteinuria. Gain insights to improve maternal and fetal outcomes. ... c) Fetal prognosis according to maternal proteinuria: We recorded 204 children born to mothers with proteinuria greater than or ... c) Fetal prognosis according to maternal proteinuria: We recorded 204 children born to mothers with proteinuria greater than or ... We recorded 204 children born with mothgers with proteinuria greater than or equal to 30 mg/dl, or 80% of children. 30 cases of ...
Proteinuria was heaviest during pregnancy in all patients. One woman was biopsied during pregnancy and 8 were biopsied ... Only 104 (57%) women had urine tested in centre postnatally, 47(50%) of these women had continued proteinuria at the time of ... Proteinuria at booking may be a clue to underlying renal disease but isnt always present. ... Significant renal disease was newly diagnosed in 9(10%), of these, only 3 had significant proteinuria at booking. Follow-up ...
Synonyms (terms occurring on more labels are shown first): proteinuria, urine protein present, proteinuria present, protein- ... Proteinuria. Definition: A disorder characterized by laboratory test results that indicate the presence of excessive protein in ...
Initial screening for proteinuria by urine dipstick test (UDT) may be useful for predicting clinical outcomes. The Shinken ... Role of dipstick proteinuria for predicting cardiovascular events: a Japanese cardiovascular hospital database analysis.. Apr 6 ... Initial screening for proteinuria by urine dipstick test (UDT) may be useful for predicting clinical outcomes. The Shinken ... The incidence of all-cause death, HF and IS events increased significantly from negative to trace to positive proteinuria ...
The prevalence of proteinuria in patients presenting acutely with oedema due to heart failure has not been studied extensively ... The prevalence of proteinuria in patients presenting acutely with oedema due to heart failure has not been studied extensively ... The prevalence of proteinuria in patients presenting with fluid retention due to heart failure ... A random collection of urine albumin-creatinine ratios (ACRs) in successive patients was used to quantify proteinuria. Out of a ...
Increasing levels of proteinuria is considered to be associated with adverse maternal and fetal outcomes. We aim to determine ... Measure of proteinuria is a poor predictor of either maternal or fetal complications in women with pre-eclampsia. ... Sixteen primary articles with a total of 6749 women met the selection criteria with levels of proteinuria estimated by urine ... All 10 studies predicting maternal outcomes showed that proteinuria is a poor predictor of maternal complications in women with ...
Background: Hypertension and proteinuria are critically involved in the progression of chronic kidney disease. Despite ... Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: a systematic review ... 2016) Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: a systematic ...
The evidence presented indicates clearly that the feeding of colostrum is responsible for the proteinuria. Observations on many ... PROTEINURIA IN NEW-BORN CALVES FOLLOWING THE FEEDING OF COLOSTRUM Theobald Smith, Theobald Smith ... Theobald Smith, Ralph B. Little; PROTEINURIA IN NEW-BORN CALVES FOLLOWING THE FEEDING OF COLOSTRUM . J Exp Med 1 February 1924 ... In the two cases fed repeatedly with colostrum, proteinuria was demonstrated up to 6 days in one case. The regularity of its ...
Keywords: Renal failure, proteinuria, copper, zinc, magnesium.. T. Tetiker, S. Paydas, G. Y regir, Y. Sagl ker. Trace Elements ... Trace Elements Alterations in Chronic Hemodialysis Patients with Chronic Renal Failure and Proteinuria. T. Tetiker, S. Paydas, ... Alterations in Chronic Hemodialysis Patients with Chronic Renal Failure and Proteinuria. Med J Islamic World Acad Sci. 1993; 6( ...
Tubular and overflow proteinuria are nonglomerular (ie, nonalbumin) forms of proteinuria. If urine dipsticks are specific for ... encoded search term (Proteinuria) and Proteinuria What to Read Next on Medscape ... Proteinuria Differential Diagnoses. Updated: Nov 14, 2014 * Author: Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF; ... The role of proteinuria in the progression of chronic renal failure. Am J Kidney Dis. 1996 Jun. 27(6):765-75. [QxMD MEDLINE ...
Foamy urine is considered a cardinal sign of proteinuria, but only a third of people with foamy urine have proteinuria as the ... People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and ... Proteinuria is the presence of excess proteins in the urine.[2] This can result in the urine being foamy.[2] Complications can ... Proteinuria is relatively common in adults, occurring in about 20% of people.[2][3] Of those with a positive urine dipstick, ...
"Proteinuria" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Proteinuria" by people in this website by year, and whether " ... Leitão CB, Froud T, Cure P, Tharavanij T, Pileggi A, Ricordi C, Alejandro R. Nonalbumin proteinuria in islet transplant ... Sgambat K, Banks M, Moudgil A. Effect of galactose on glomerular permeability and proteinuria in steroid-resistant nephrotic ...
When exposed to theoretical scenarios of proteinuria in dogs with CanL at stages IIb, III and IV (LeishVet guidelines), 16.3%, ... Among the veterinary practitioners who responded, proteinuria treatment was considered since stage IIb CanL, although ... little information is available on which treatments are most adequate for identifying proteinuria in patients with canine ... included the general features of the respondents and the protocols preferred by these respondents to manage proteinuria in the ...
Proteinuria is an increased level of protein in the urine. We look at the causes of proteinuria, its connection with kidney ... Additionally, some individuals may have proteinuria in the day but not at night. This may indicate orthostatic proteinuria. , ... The term proteinuria describes an excessive level of protein in the urine. The presence of protein in the urine beyond a ... Everything you need to know about protein in urine (proteinuria). Medically reviewed by Lauren Castiello, RN ...
Cao, X., Wei, R., Zhou, J. et al. Wenshen Jianpi recipe, a blended traditional Chinese medicine, ameliorates proteinuria and ... Proteinuria and the expression of the podocyte slit diaphragm protein, nephrin, in diabetic nephropathy: effects of angiotensin ... Wenshen Jianpi recipe, a blended traditional Chinese medicine, ameliorates proteinuria and renal injury in a rat model of ... Wenshen Jianpi recipe, a blended traditional Chinese medicine, ameliorates proteinuria and renal injury in a rat model of ...
  • Types that do not result from pathological damage to the glomerulus include transient and orthostatic proteinuria. (medscape.com)
  • Orthostatic proteinuria is diagnosed if the patient has no proteinuria in early morning samples but has low-grade proteinuria at the end of the day. (medscape.com)
  • Springberg PD, Garrett LE Jr, Thompson AL Jr. Fixed and reproducible orthostatic proteinuria: results of a 20-year follow-up study. (medscape.com)
  • Orthostatic proteinuria occurs in between 2-5% of all adolescents-it is primarily a pediatric condition, rarely occurring after age 30. (renalfellow.org)
  • I use the term "condition" rather than "disease" because orthostatic proteinuria carries with it a benign prognosis with no danger of worsening renal function. (renalfellow.org)
  • In order to make a diagnosis of orthostatic proteinuria, one can obtain either a 24-hour urine collection, or one can do it using separate urine protein/creatinine ratios. (renalfellow.org)
  • In order for a diagnosis of orthostatic proteinuria to be made, there must be abnormal proteinuria (e.g., >100mg/16 hrs) during the upright collection but normal urine protein (e.g., during the overnight collection. (renalfellow.org)
  • What is the pathogenesis of orthostatic proteinuria? (renalfellow.org)
  • Orthostatic proteinuria is a benign condition (most common among children and adolescents) in which proteinuria occurs mainly when the patient is upright. (msdmanuals.com)
  • Proteinuria is usually benign, in the form of transient or orthostatic proteinuria. (medbullets.com)
  • This is called orthostatic Proteinuria and it does not cause any harm. (planetayurveda.net)
  • The nutcracker syndrome is the congestion of left renal vein due to the compression of left renal vein by the aorta and the superior mesenteric artery and has been known as tile cause of hematuria with or without left renal flank pain, mild to moderate proteinuria and orthostatic proteinuria. (chikd.org)
  • There is also preliminary evidence that higher levels of proteinuria correlate with reduced survival times in cats with or without renal failure. (vin.com)
  • Up to 30% of people who have IgAN with persistent higher levels of proteinuria (≥1 g/day) progress to kidney failure within 10 years 6 . (novartis.com)
  • However, immunosuppression induced more full clinical remissions in particular in patients with lower levels of proteinuria. (medscape.com)
  • A community based cohort study done of adults for mean follow up of 35 months showed that the risks for all cause mortality, heart attacks, progression to kidney failure associated with a given level of GFR were independently increased among patients with higher levels of proteinuria. (nephronpower.com)
  • For example, paraprotein deposition can induce a glomerulopathy leading to the additional loss of albumin and more profound proteinuria. (medscape.com)
  • [2] [4] Proteinuria is defined as a urine protein creatinine ratio (UPCR) of more than 45 to 50 mg/mmol (400 mg/g to 440 mg/g) or a urine albumin creatinine ratio (UACR) of greater than 30 mg/mmol. (mdwiki.org)
  • Proteinuria is protein, usually albumin , in urine. (msdmanuals.com)
  • Albuminuria as a noun is the presence of albumin in the urine, often a symptom of renal disease while Proteinuria as a noun is excessive protein in the urine. (differencebee.com)
  • Actually, the best way to analyze Ayurvedic treatment for proteinuria is a protein in the pee test. (tutorialspoint.com)
  • Proteinuria may be a feature of the following conditions: Nephrotic syndromes (i.e. intrinsic kidney failure) Pre-eclampsia Eclampsia Toxic lesions of kidneys Amyloidosis Collagen vascular diseases (e.g. systemic lupus erythematosus) Dehydration Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis) Strenuous exercise Stress Benign orthostatic (postural) proteinuria Focal segmental glomerulosclerosis (FSGS) IgA nephropathy (i.e. (wikipedia.org)
  • The lower incidence and relatively benign nature of proteinuria seen in this review support previous findings that auranofin is better tolerated than injectable gold. (nih.gov)
  • Proteinuria is common in children and may represent a benign condition or a serious underlying renal disease or systemic disorder. (medbullets.com)
  • In many cases, proteinuria is caused by relatively benign (non-cancerous) or temporary medical conditions. (apnaupchar.com)
  • Overflow proteinuria occurs when excessive amounts of small plasma proteins (eg, immunoglobulin light chains produced in multiple myeloma) exceed the reabsorptive capacity of the proximal tubules. (msdmanuals.com)
  • Nephrotic-range proteinuria is defined as greater than 3.5 g of protein excreted in the urine over 24 hours. (medscape.com)
  • In the presence of stable renal function, a protein/creatinine ratio of more than 3.5 (mg/mg) can be taken to represent "nephrotic-range" proteinuria, and a ratio of less than 0.2 is within normal limits. (nih.gov)
  • The bigger question at debate is also:- is non nephrotic range proteinuria all bad? (nephronpower.com)
  • We conclude that the determination of the protein/creatinine ratio in single urine samples obtained during normal daylight activity, when properly interpreted by taking into consideration the effect of different rates of creatinine excretion, can replace the 24-hour urine collection in the clinical quantitation of proteinuria. (nih.gov)
  • To investigate association between maternofoetal complications and the amount of proteinuria measured by spot urine protein creatinine ratio in patients with preeclampsia. (hindawi.com)
  • Proteinuria may be measured quantitatively over 24 hours, or more simply by a random urine protein to creatinine (UPC) ratio (the two showing a close correlation in both humans and cats). (vin.com)
  • In this study, proteinuria was assessed in 100 randomly selected sick cats and 22 healthy cats by means of the urine protein:creatinine ratio, a traditional urine 'dipstick' and a commercial ELISA-based dipstick designed to detect microalbuminuria (MA) semi-quantitatively. (vin.com)
  • Random spot urine protein/creatinine ratio is unreliable for estimating 24-Hour proteinuria in individual systemic lupus erythematosus nephritis patients. (medscape.com)
  • Of those, 1016 had both preoperative creatinine and proteinuria measurements available. (cancertherapyadvisor.com)
  • Laboratory findings include low platelets, elevated white blood cell counts, electrolyte abnormalities, elevated blood urea nitrogen (BUN) and creatinine, and proteinuria. (cdc.gov)
  • The study met its primary efficacy endpoint at the 36-week interim analysis, with atrasentan demonstrating superiority versus placebo with a clinically meaningful and highly statistically significant reduction in proteinuria (protein in urine) in patients with IgAN receiving supportive care (maximally tolerated and stable dose of a renin-angiotensin system [RAS] inhibitor) 1 . (novartis.com)
  • This is the most sensitive in detecting small amounts of protein in urine and is helpful in detecting early proteinuria. (indevets.com)
  • In human beings, most cases of renal failure occur secondary to diabetes mellitus or essential hypertension, and there is considerable interest in the potential role of proteinuria as a cause, as well as an indicator, of progressive renal damage. (vin.com)
  • The role of proteinuria in the progression of chronic renal failure. (medscape.com)
  • The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field. (wikipedia.org)
  • Diabetes is the greatest cause of proteinuria. (tutorialspoint.com)
  • Clinical features from the history, physical examination, and laboratory tests help determine the cause of proteinuria. (medbullets.com)
  • A couple of studies have also been done to find out association between the amount of proteinuria and maternofoetal outcome in patients with preeclampsia but the results have been variable [ 9 - 11 ]. (hindawi.com)
  • This study was carried out in patients with preeclampsia to estimate the prevalence of maternal and foetal morbidity and to investigate the association between the amount of proteinuria measured by spot UPCR and maternofoetal outcome. (hindawi.com)
  • There was a generally positive association between arsenic and albuminuria and proteinuria outcomes. (cdc.gov)
  • Assessment of a small number of studies with three or more categories showed a clear dose-response association between arsenic and prevalent albuminuria and proteinuria, but not with CKD outcomes. (cdc.gov)
  • Background: Hypertension and proteinuria are critically involved in the progression of chronic kidney disease. (gla.ac.uk)
  • Preeclampsia is the simultaneous development of hypertension and proteinuria in a pregnant woman. (apnaupchar.com)
  • Proteinuria often causes no symptoms and it may only be discovered incidentally. (wikipedia.org)
  • What are the causes and symptoms of Proteinuria? (tutorialspoint.com)
  • Proteinuria often doesn't cause any symptoms and it may be discovered incidentally. (mdwiki.org)
  • Isolated proteinuria is urinary protein without other symptoms or urinary abnormalities. (msdmanuals.com)
  • It has a prophylactic activity and controls the symptoms of proteinuria effectively. (planetayurveda.net)
  • Does Proteinuria Cause Symptoms? (kidneyhealth.com.sg)
  • Proteinuria may not cause any noticeable symptoms in some individuals but in other individuals, causes a wide variety of symptoms, depending on the underlying cause and the seriousness of the condition. (kidneyhealth.com.sg)
  • One of the most common symptoms of proteinuria is the appearance of foamy or bubbly urine. (kidneyhealth.com.sg)
  • Urinary mercury excretion and proteinuria in pathology laboratory staff. (bmj.com)
  • Proteinuria (in the absence of lower urinary tract disease) is therefore usually a marker of renal damage or dysfunction (glomerular or tubular), although this may result from either primary or secondary renal disease. (vin.com)
  • In addition, a kidney stone in the urinary tract can cause proteinuria. (apnaupchar.com)
  • Urine infection may also cause proteinuria, but usually there some other signs related to it- such as Cystitis or any other urinary tract infections. (planetayurveda.net)
  • The annual urinary screening of Japanese children above 3 yr of age has identified a progressive proximal renal tubular disorder characterized by low molecular weight proteinuria, hypercalciuria, and nephrocalcinosis. (ox.ac.uk)
  • This reduction was associated with the disappearance of trace proteinuria from the technicians' urine. (bmj.com)
  • Even trace proteinuria was independently associated with HF (HR: 1.64, 95% CI 1.07-2.53) and IS (HR: 2.17, 95% CI 1.14-4.11) and with all-cause death (HR: 1.56, 95% CI 0.99-2.47). (physiciansweekly.com)
  • Amiloride, an epithelial sodium channel (ENaC) inhibitor, was reported to reduce proteinuria in animal studies and case reports independent of ENaC inhibition. (karger.com)
  • We hypothesized that amiloride not triamterene (an analog of amiloride) would reduce proteinuria in the patients with proteinuric kidney disease. (karger.com)
  • In previous studies, "ACE inhibitors were widely used to reduce proteinuria. (medscape.com)
  • Tubular proteinuria is a result of tubulointersitial disease affecting the proximal renal tubules and interstitium. (medscape.com)
  • Diseases that interfere with proximal tubular function, such as tubulointerstitial nephritis, reduce reabsorption of these proteins and lead to tubular proteinuria. (medscape.com)
  • There are three main mechanisms to cause proteinuria:[citation needed] Due to disease in the glomerulus Because of increased quantity of proteins in serum (overflow proteinuria) Due to low reabsorption at proximal tubule (Fanconi syndrome) Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. (wikipedia.org)
  • Overflow proteinuria is most commonly associated with increased production of abnormal low molecular weight proteins (eg, light chains in multiple myeloma, myoglobin in rhabdomyolysis) that exceeds the reabsorption capacity of the proximal tubule, leading to spilling of the protein into the urine. (medscape.com)
  • Tubular and overflow proteinuria are nonglomerular (ie, nonalbumin) forms of proteinuria. (medscape.com)
  • Overflow proteinuria almost always is caused by excess production of immunoglobulin light chains, such as that associated with multiple myeloma or monoclonal gammopathy of uncertain significance (MGUS). (medscape.com)
  • Overflow proteinuria is a common sign of certain medical conditions, such as multiple myeloma or amyloidosis. (kidneyhealth.com.sg)
  • Role of dipstick proteinuria for predicting cardiovascular events: a Japanese cardiovascular hospital database analysis. (physiciansweekly.com)
  • In conclusions, dipstick proteinuria was independently associated with cardiovascular events and death, suggesting that the UDT is a useful tool for evaluating patients' risk for such adverse events. (physiciansweekly.com)
  • 0.4-0.5 is accepted as abnormal proteinuria. (vin.com)
  • In the present study, preeclampsia was diagnosed in patients who had resting blood pressure equal to or more than 140/90 mmHg at two different occasions at least 4 hours apart with significant proteinuria detected in urine samples (defined as more than or equal to 300 mg/24 hrs or spot UPCR 0.3 gm/gm in random urine sample). (hindawi.com)
  • Significant renal disease was newly diagnosed in 9(10%), of these, only 3 had significant proteinuria at booking. (bmj.com)
  • Proteinuria identifies patients with kidney damage and those at risk for worsening kidney disease and increased cardiovascular morbidity. (medscape.com)
  • Treatment records of 1800 patients with rheumatoid arthritis who were included in the clinical trials of auranofin in the United States were examined for data on development of proteinuria. (nih.gov)
  • Three percent (41) of 1283 auranofin-treated patients had an abnormal 24-hour urine protein level: 15 had mild (0.15 to 1 g/d), 17 had moderate (1 to 3.5 g/d), and 9 had heavy (greater than 3.5 g/d) proteinuria. (nih.gov)
  • Permanent renal impairment did not occur, and proteinuria did not persist beyond 12 months in most patients. (nih.gov)
  • Seven of eight patients who were rechallenged when the proteinuria had cleared were able to continue treatment without relapse. (nih.gov)
  • In similar groups of patients, the risk of developing proteinuria with auranofin therapy is significantly less than that with parenteral gold therapy (p less than 0.05) and similar to that with background therapy with nonsteroidal antiinflammatory drugs (p = 0.92). (nih.gov)
  • These positive topline Phase III data showcase the potential of atrasentan to improve outcomes for patients with IgAN by demonstrating clinically meaningful proteinuria reduction," said Shreeram Aradhye, M.D., President, Development and Chief Medical Officer, Novartis. (novartis.com)
  • Approximately 340 patients with biopsy-proven IgAN with baseline total proteinuria over one gram per day despite optimized RAS inhibitor treatment were randomized to receive once-daily oral doses of atrasentan (0.75 mg) or placebo for approximately 2.5 years (132 weeks) 11,12 . (novartis.com)
  • Both amiloride and triamterene significantly reduced proteinuria in patients with proteinuric kidney disease. (karger.com)
  • Proteinuria was heaviest during pregnancy in all patients. (bmj.com)
  • Patients for whom UDT was performed at their initial visit between 2004 and 2010 (n = 7131) were divided into three groups according to the test results: negative, trace, and positive (1+ to 4+) proteinuria. (physiciansweekly.com)
  • Although antileishmanial therapeutic protocols are widely implemented, little information is available on which treatments are most adequate for identifying proteinuria in patients with canine leishmaniosis (CanL), especially regarding the use of immunosuppressants. (biomedcentral.com)
  • Proteinuria is a predictor for renal functional decline in patients with kidney cancer , a study published in The Journal of Urology has shown. (cancertherapyadvisor.com)
  • Although prior studies have demonstrated that 26% to 34% of patients with suspected kidney cancers have a glomerular filtration rate (GFR) less than 60 mL/min/1.73 m 2 , there are limited data on the incidence of proteinuria. (cancertherapyadvisor.com)
  • Therefore, researchers sought to investigate the extent of proteinuria in patients with kidney cancer to determine the impact on classification and progression of chronic kidney disease (CKD). (cancertherapyadvisor.com)
  • Proteinuria is a predictor of renal functional decline in kidney cancer patients [published online ahead of print March 23, 2016]. (cancertherapyadvisor.com)
  • But by simply optimizing supportive care - getting blood pressure and proteinuria down to optimal levels and doing a lot of things we can do to help preserve kidney function conservatively - we saved patients from the need for immunosuppression," Dr Floege reported. (medscape.com)
  • The remaining 162 patients with persistent proteinuria, defined as more than 0.75 g/day of protein in the urine, were randomized to supportive therapy alone or to supportive therapy plus immunosuppression for 3 years. (medscape.com)
  • Therefore, if proteinuria persists, immunosuppression might be considered an option in patients with early-stage disease whose proteinuria levels do not exceed 1.5 g/day, said Dr Floege. (medscape.com)
  • The aim of this study was to validate proteinuria as a predictor of long-term renal outcome in real-life situation in a racially diverse group of patients with severe nephritis. (bmj.com)
  • The proteinuria cut-off value of 0.8 g/24 hours at 12 months was a good predictor of 7-year renal survival (years free of dialysis) for patients with pure membranous (p=0.005) and proliferative nephritis (p=0.043), as well as black (p=0.002) and white race (p=0.001), anti-dsDNA positive (p=0.001) and anti-dsDNA negative (p=0.04) and male (p=0.028) and female (p=0.003) patients. (bmj.com)
  • Conclusion We provided novel evidence that, in a real-life situation, proteinuria at 12 months of follow-up was the single best predictor of renal outcome at 7 years for an ethnically diverse group of patients with severe nephritis and a valid parameter for distinct histological classes, races, genders and anti-dsDNA profiles. (bmj.com)
  • Proteinuria is a sign therefore that the kidneys have become damaged. (apnaupchar.com)
  • In cases of kidney disease, proteinuria is a sign that the pet's kidneys are not filtering waste from the bloodstream or balancing levels of important nutrients and is associated with a poorer prognosis. (indevets.com)
  • The 2021 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for evaluating and managing chronic kidney disease (CKD) includes proteinuria in the staging of CKD. (medscape.com)
  • Proteinuria is a major determinant of progression of chronic kidney disease (CKD), which is associated with more rapid worsening of renal function and earlier initiation of renal replacement therapy independent of estimated glomerular filtration rate (eGFR) [ 1 ]. (karger.com)
  • Preclinical data have shown that in models of rare chronic kidney disease this activity reduces proteinuria , protects podocytes, and prevents glomerulosclerosis and mesangial cell proliferation. (medscape.com)
  • Occasionally, proteinuria is an early indication of chronic kidney disease, a gradual loss of kidney function that may eventually require dialysis or a kidney transplant. (apnaupchar.com)
  • In cases where proteinuria is related to conditions other than kidney disease, the proteinuria will resolve when the underlying condition is treated. (indevets.com)
  • Non-selective proteinuria is a common sign of kidney disease and can occur in multiple medical conditions. (kidneyhealth.com.sg)
  • Krishnan A, Levin A. Laboratory assessment of kidney disease: glomerular filtration rate, urinalysis, and proteinuria. (medlineplus.gov)
  • If you have temporary or mild proteinuria, you likely won't need treatment. (apnaupchar.com)
  • Transient proteinuria occurs in persons with normal kidney function, bland urine sediment, and normal blood pressure. (medscape.com)
  • In the veterinary field, significant renal-origin proteinuria has been demonstrated in association with a variety of underlying conditions in dogs, and there is evidence to suggest that in cases of canine chronic renal failure, proteinuria is a negative prognostic indicator, with a number of recent studies also evaluating MA in dogs. (vin.com)
  • Proteinuria has been shown to occur in cats with immune-mediated glomerulonephritis, multiple myeloma, acute renal failure, chronic renal failure, hyperthyroidism acute pancreatitis, drug reactions and hypertension. (vin.com)
  • Proteinuria is a chronic ailment and once in a while does it demonstrate any manifestations amid the beginning periods. (tutorialspoint.com)
  • Ruggenenti P, Perna A, Mosconi L. Proteinuria predicts end-stage renal failure in non-diabetic chronic nephropathies. (medscape.com)
  • How Does TCM Treat Proteinuria of Chronic Nephritis? (tcm-nephritis.com)
  • The objectives of this work were to calculate the frequency of arterial hypertension during pregnancy, describe the epidemiological profile, and identify the most common type of hypertension and to establish fetal prognosis based on uricemia and maternal proteinuria. (scirp.org)
  • It must be aware that proteinuria plays a vital role in the development and prognosis of renal disease. (tcm-nephritis.com)
  • An individual with proteinuria in the setting of a regular glomerular filtration rate (GFR) is at high risk of progressive loss of kidney function. (medscape.com)
  • Around 6 years ago, his estimated glomerular filtration rate (eGFR) was 50 mL/min/1.73 m 2 with 6 g for proteinuria when referred to nephrology. (medscape.com)
  • Proteinuria is the presence of excess proteins in the urine. (wikipedia.org)
  • Proteins Secreted by Lung Cancer Cells Induce the Onset of Proteinuria via Focal Adhesion Kinase Signaling in Mice. (bvsalud.org)
  • Proteinuria caused by renal disorders usually is persistent (ie, present on serial testing) and, when in the nephrotic range, can cause significant protein wasting. (msdmanuals.com)
  • Persistent proteinuria may be associated with more serious renal diseases. (medbullets.com)
  • Early proteinuria response: a valid real-life situation predictor of long-term lupus renal outcome in an ethnically diverse group with severe biopsy-proven nephritis? (bmj.com)
  • Objective Two recent important lupus nephritis trials reported that proteinuria was a good predictor of renal outcome in Caucasians, but data on real-life situation, other races and severe nephritis are lacking to substantiate this finding as a simple test to guide clinical practice. (bmj.com)
  • A simple urine test, known as a urinalysis, is usually the first step in diagnosing proteinuria. (kidneyhealth.com.sg)
  • Initial laboratory data include a urinalysis showing 3+ proteinuria and glycosuria. (cdc.gov)
  • Smaller losses are within normal ranges and greater losses are detectable by the UPC ratio (overt proteinuria). (vin.com)
  • Multivariate analysis revealed independent association between proteinuria and all-cause death [hazard ratio (HR): 1.50, 95% confidence interval (CI) 1.07-2.10], HF (HR: 1.55, 95% CI 1.14-2.12), and IS (HR: 2.08, 95% CI 1.26-3.45). (physiciansweekly.com)
  • Urine Protein Creatnine Ratio (UPC) - quantifies proteinuria. (indevets.com)
  • People with diabetes may have damaged nephrons and develop proteinuria. (wikipedia.org)
  • Under the urging of Lei Zhentian treatment of proteinuria in diabetic nephropathy when hyperkalemic and the Thirteenth Taibao, the winding snake formation composed of tens of thousands of people slowly moved forward in the wetland swampMarch Jekyll, did you notice that the wetland swamp. (moviebill.com)
  • At this time, Zhu Bin, a war madman who is already known as Hitler in the world, will never let him go This is a good opportunity for his feats to reach new heights The army of more than one million people staying in the north and the torrent of steel gathered treatment of proteinuria in diabetic nephropathy when hyperkalemic will surely roll forward. (moviebill.com)
  • Adding me, there are still one hundred and treatment of proteinuria in diabetic nephropathy when hyperkalemic twenty-three people in the whole town Half a month ago, the number was twice this number, but because of an air strike by the National Defense Forces, most of them. (moviebill.com)
  • Severe proteinuria can cause nephrotic syndrome in which there is worsening swelling of the body. (wikipedia.org)
  • citation needed] With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. (wikipedia.org)
  • the more severe the proteinuria, the more significant the glomerular disease. (medscape.com)
  • If left untreated, proteinuria can lead to more severe complications, such as kidney failure. (kidneyhealth.com.sg)
  • Proteinuria can also be a symptom of some other diseases: for example congestive heart failure or if a woman had eclampsia during pregnancy. (planetayurveda.net)
  • High blood pressure, or hypertension, can be a symptom of proteinuria. (kidneyhealth.com.sg)
  • However, there was no correlation between serum adiponectin and proteinuria or estradiol and progesterone levels. (who.int)
  • Caughey, AB 2008, ' Predicting proteinuria in pregnancy: A potential algorithm ', Journal of Perinatology , vol. 28, no. 7, pp. 451-452. (elsevierpure.com)
  • Corrigendum to "The feasibility and acceptability of self-testing for proteinuria during pregnancy: A mixed methods approach" [Pregn. (ox.ac.uk)
  • Endothelin also directly acts on podocytes, where it can promote slit diaphragm and cytoskeletal disruption, podocyte loss, and proteinuria-actions that characterize FSGS. (medtelligence.net)
  • citation needed] Foamy urine is considered a cardinal sign of proteinuria, but only a third of people with foamy urine have proteinuria as the underlying cause. (wikipedia.org)
  • These tests can help identify any abnormalities or blockages contributing to proteinuria. (kidneyhealth.com.sg)
  • Idiopathic low molecular weight proteinuria associated with hypercalciuric nephrocalcinosis in Japanese children is due to mutations of the renal chloride channel (CLCN5). (ox.ac.uk)