Glomerular filtration rate. Medical search

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.

Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.

Laboratory tests used to evaluate how well the kidneys are working through examination of blood and urine.

Pathological processes of the KIDNEY or its component tissues.

An extracellular cystatin subtype that is abundantly expressed in bodily fluids. It may play a role in the inhibition of interstitial CYSTEINE PROTEASES.

A starch found in the tubers and roots of many plants. Since it is hydrolyzable to FRUCTOSE, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function.

The circulation of the BLOOD through the vessels of the KIDNEY.

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)

A technetium imaging agent used in renal scintigraphy, computed tomography, lung ventilation imaging, gastrointestinal scintigraphy, and many other procedures which employ radionuclide imaging agents.

A contrast medium in diagnostic radiology with properties similar to those of diatrizoic acid. It is used primarily as its sodium and meglumine (IOTHALAMATE MEGLUMINE) salts.

The presence of albumin in the urine, an indicator of KIDNEY DISEASES.

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.

Sodium excretion by URINATION.

The presence of proteins in the urine, an indicator of KIDNEY DISEASES.

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.

An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)

A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.

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.

PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.

The amount of PLASMA that perfuses the KIDNEYS per unit time, approximately 10% greater than effective renal plasma flow (RENAL PLASMA FLOW, EFFECTIVE). It should be differentiated from the RENAL BLOOD FLOW; (RBF), which refers to the total volume of BLOOD flowing through the renal vasculature, while the renal plasma flow refers to the rate of plasma flow (RPF).

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.

A homologous group of endogenous CYSTEINE PROTEINASE INHIBITORS. The cystatins inhibit most CYSTEINE ENDOPEPTIDASES such as PAPAIN, and other peptidases which have a sulfhydryl group at the active site.

The functional units of the kidney, consisting of the glomerulus and the attached tubule.

A process of separating particulate matter from a fluid, such as air or a liquid, by passing the fluid carrier through a medium that will not pass the particulates. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

An effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality.

Graphic tracing over a time period of radioactivity measured externally over the kidneys following intravenous injection of a radionuclide which is taken up and excreted by the kidneys.

A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.

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.

Unstable isotopes of chromium that decay or disintegrate emitting radiation. Cr atoms with atomic weights of 46-49, 51, 55, and 56 are radioactive chromium isotopes.

Excision of kidney.

The transference of a kidney from one human or animal to another.

Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.

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.

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 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.

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.

The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.

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.

Volume of biological fluid completely cleared of drug metabolites as measured in unit time. Elimination occurs as a result of metabolic processes in the kidney, liver, saliva, sweat, intestine, heart, brain, or other site.

The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.

Narrowing or occlusion of the RENAL ARTERY or arteries. It is due usually to ATHEROSCLEROSIS; FIBROMUSCULAR DYSPLASIA; THROMBOSIS; EMBOLISM, or external pressure. The reduced renal perfusion can lead to renovascular hypertension (HYPERTENSION, RENOVASCULAR).

A group of glycine amides of aminobenzoic acids.

Elements of limited time intervals, contributing to particular results or situations.

A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.

A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.

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 amount of PLASMA flowing to the parts of the KIDNEY that function in the production of urine. It is the amount of plasma perfusing the KIDNEY TUBULES per unit time, generally measured by P-AMINOHIPPURATE clearance. It should be differentiated from RENAL PLASMA FLOW which is approximately 10% greater than the effective renal plasma flow.

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.

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.

Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.

The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)

Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.

Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with LONGITUDINAL STUDIES which are followed over a period of time.

A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.

Liquid by-product of excretion produced in the kidneys, temporarily stored in the bladder until discharge through the URETHRA.

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.

Incision of tissues for injection of medication or for other diagnostic or therapeutic procedures. Punctures of the skin, for example may be used for diagnostic drainage; of blood vessels for diagnostic imaging procedures.

In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.

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.

The balance of fluid in the BODY FLUID COMPARTMENTS; total BODY WATER; BLOOD VOLUME; EXTRACELLULAR SPACE; INTRACELLULAR SPACE, maintained by processes in the body that regulate the intake and excretion of WATER and ELECTROLYTES, particularly SODIUM and POTASSIUM.

The physical or physiological processes by which substances, tissue, cells, etc. take up or take in other substances or energy.

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.

An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.

Substances that dissociate into two or more ions, to some extent, in water. Solutions of electrolytes thus conduct an electric current and can be decomposed by it (ELECTROLYSIS). (Grant & Hackh's Chemical Dictionary, 5th ed)

The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.

The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.

Agents that promote the excretion of urine through their effects on kidney function.

The ability of the kidney to excrete in the urine high concentrations of solutes from the blood plasma.

A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.

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.

Volume of PLASMA in the circulation. It is usually measured by INDICATOR DILUTION TECHNIQUES.

Hypertension due to RENAL ARTERY OBSTRUCTION or compression.

A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.

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.

An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.

The two dimensional measure of the outer layer of the body.

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.

A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.

A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.

The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.

A diverse family of extracellular proteins that bind to small hydrophobic molecules. They were originally characterized as transport proteins, however they may have additional roles such as taking part in the formation of macromolecular complexes with other proteins and binding to CELL SURFACE RECEPTORS.

The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)

Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.

The qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences. (Last, Dictionary of Epidemiology, 1988)

The mechanical laws of fluid dynamics as they apply to urine transport.

Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.

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 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.

Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.

A ubiquitous sodium salt that is commonly used to season food.

The flow of BLOOD through or around an organ or region of the body.

An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.

The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per liter of solution. Osmolality is expressed in terms of osmoles of solute per kilogram of solvent.

Condition where a primary dysfunction of either heart or kidney results in failure of the other organ (e.g., HEART FAILURE with worsening RENAL INSUFFICIENCY).

The portion of renal tubule that begins from the enlarged segment of the ascending limb of the LOOP OF HENLE. It reenters the KIDNEY CORTEX and forms the convoluted segments of the distal tubule.

An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.

The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.

An iodine-containing compound used in pyelography as a radiopaque medium. If labeled with radioiodine, it can be used for studies of renal function.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

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.

A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.

Short thick veins which return blood from the kidneys to the vena cava.

A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.

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).

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.

Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.

A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.

The volume of packed RED BLOOD CELLS in a blood specimen. The volume is measured by centrifugation in a tube with graduated markings, or with automated blood cell counters. It is an indicator of erythrocyte status in disease. For example, ANEMIA shows a low value; POLYCYTHEMIA, a high value.

Substances used to allow enhanced visualization of tissues.

Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.

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.

Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.

An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.

A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney.

Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression.

Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.

Statistical models used in survival analysis that assert that the effect of the study factors on the hazard rate in the study population is multiplicative and does not change over time.

A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables.

The internal portion of the kidney, consisting of striated conical masses, the renal pyramids, whose bases are adjacent to the cortex and whose apices form prominent papillae projecting into the lumen of the minor calyces.

A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.

Discharge of URINE, liquid waste processed by the KIDNEY, from the body.

Excessive URIC ACID or urate in blood as defined by its solubility in plasma at 37 degrees C; greater than 0.42mmol per liter (7.0mg/dL) in men or 0.36mmol per liter (6.0mg/dL) in women. This condition is caused by overproduction of uric acid or impaired renal clearance. Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with HYPERTENSION and GOUT.

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.

The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.

A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.

Blockage in any part of the URETER causing obstruction of urine flow from the kidney to the URINARY BLADDER. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as HYDRONEPHROSIS and obstructive nephropathy.

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

The pressure due to the weight of fluid.

An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.

Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see LINEAR MODELS) the relationship is constrained to be a straight line and LEAST-SQUARES ANALYSIS is used to determine the best fit. In logistic regression (see LOGISTIC MODELS) the dependent variable is qualitative rather than continuously variable and LIKELIHOOD FUNCTIONS are used to find the best relationship. In multiple regression, the dependent variable is considered to depend on more than a single independent variable.

The measurement of an organ in volume, mass, or heaviness.

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 polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.

A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.

Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.

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.

Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)

A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.

A nonparametric method of compiling LIFE TABLES or survival tables. It combines calculated probabilities of survival and estimates to allow for observations occurring beyond a measurement threshold, which are assumed to occur randomly. Time intervals are defined as ending each time an event occurs and are therefore unequal. (From Last, A Dictionary of Epidemiology, 1995)

Endogenous or exogenous chemicals that regulate the WATER-ELECTROLYTE BALANCE in the body. They consist of peptides and non-peptide compounds.

The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from PREVALENCE, which refers to all cases, new or old, in the population at a given time.

A commonly used x-ray contrast medium. As DIATRIZOATE MEGLUMINE and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography.

An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.

A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.

Triiodo-substituted derivatives of BENZOIC ACID.

An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.

The U-shaped portion of the renal tubule in the KIDNEY MEDULLA, consisting of a descending limb and an ascending limb. It is situated between the PROXIMAL KIDNEY TUBULE and the DISTAL KIDNEY TUBULE.

A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.

Individuals whose ancestral origins are in the southeastern and eastern areas of the Asian continent.

Treatment process involving the injection of fluid into an organ or tissue.

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.

A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.

The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host.

The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival.

Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.

A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)

A pathological condition that removes acid or adds base to the body fluids.

The administration of liquid medication, nutrient, or other fluid through some other route than the alimentary canal, usually over minutes or hours, either by gravity flow or often by infusion pumping.

The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.

An 11-kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants.

A distribution in which a variable is distributed like the sum of the squares of any given independent random variable, each of which has a normal distribution with mean of zero and variance of one. The chi-square test is a statistical test based on comparison of a test statistic to a chi-square distribution. The oldest of these tests are used to detect whether two or more population distributions differ from one another.

The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.

A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.

Non-cadaveric providers of organs for transplant to related or non-related recipients.

A synthetic nonapeptide (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) which is identical to the peptide from the venom of the snake, Bothrops jararaca. It inhibits kininase II and ANGIOTENSIN I and has been proposed as an antihypertensive agent.

A beta-N-Acetylhexosaminidase that catalyzes the hydrolysis of terminal, non-reducing 2-acetamido-2-deoxy-beta-glucose residues in chitobiose and higher analogs as well as in glycoproteins. Has been used widely in structural studies on bacterial cell walls and in the study of diseases such as MUCOLIPIDOSIS and various inflammatory disorders of muscle and connective tissue.

Water-soluble proteins found in egg whites, blood, lymph, and other tissues and fluids. They coagulate upon heating.

The relationship between the dose of an administered drug and the response of the organism to the drug.

The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.

The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.

A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.

A sucrose polymer of high molecular weight.

A complex of cells consisting of juxtaglomerular cells, extraglomerular mesangium lacis cells, the macula densa of the distal convoluted tubule, and granular epithelial peripolar cells. Juxtaglomerular cells are modified SMOOTH MUSCLE CELLS found in the walls of afferent glomerular arterioles and sometimes the efferent arterioles. Extraglomerular mesangium lacis cells are located in the angle between the afferent and efferent glomerular arterioles. Granular epithelial peripolar cells are located at the angle of reflection of the parietal to visceral angle of the renal corpuscle.

Injections made into a vein for therapeutic or experimental purposes.

The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.

Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)

Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.

A diet that contains limited amounts of protein. It is prescribed in some cases to slow the progression of renal failure. (From Segen, Dictionary of Modern Medicine, 1992)

Studies in which variables relating to an individual or group of individuals are assessed over a period of time.

A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.

Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

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.

Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor.

A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812)

Absence of urine formation. It is usually associated with complete bilateral ureteral (URETER) obstruction, complete lower urinary tract obstruction, or unilateral ureteral obstruction when a solitary kidney is present.

Fluids composed mainly of water found within the body.

Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.

An essential amino acid that is physiologically active in the L-form.

Conditions or pathological processes associated with the disease of diabetes mellitus. Due to the impaired control of BLOOD GLUCOSE level in diabetic patients, pathological processes develop in numerous tissues and organs including the EYE, the KIDNEY, the BLOOD VESSELS, and the NERVE TISSUE.

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.

The number of times the HEART VENTRICLES contract per unit of time, usually per minute.

A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.

Minor hemoglobin components of human erythrocytes designated A1a, A1b, and A1c. Hemoglobin A1c is most important since its sugar moiety is glucose covalently bound to the terminal amino acid of the beta chain. Since normal glycohemoglobin concentrations exclude marked blood glucose fluctuations over the preceding three to four weeks, the concentration of glycosylated hemoglobin A is a more reliable index of the blood sugar average over a long period of time.

A chronic, acquired, idiopathic, progressive eruption of the skin that occurs in the context of RENAL FAILURE. It is sometimes accompanied by systemic fibrosis. The pathogenesis seems to be multifactorial, with postulated involvement of circulating fibrocytes. There is a strong association between this disorder and the use of gadolinium-based contrast agents.

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.

Drugs used for their effects on the kidneys' regulation of body fluid composition and volume. The most commonly used are the diuretics. Also included are drugs used for their antidiuretic and uricosuric actions, for their effects on the kidneys' clearance of other drugs, and for diagnosis of renal function.

A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.

Acute renal failure caused by nephrotoxins. (1/6121)

Renal micropuncture studies have greatly changed our views on the pathophysiology of acute renal failure caused by nephrotoxins. Formerly, this type of renal insufficiency was attributed to a direct effect of the nephrotoxins on tubule epithelial permeability. According to that theory, glomerular filtration was not greatly diminished, the filtrate formed being absorbed almost quantitatively and nonselectively across damaged tubule epithelium. Studies in a wide variety of rat models have now shown glomerular filtration to be reduced to a level which will inevitably cause renal failure in and of itself. Passive backflow of filtrate across tubular epithelium is either of minor degree or nonexistent even in models where frank tubular necrosis has occurred. This failure of filtration cannot be attributed to tubular obstruction since proximal tubule pressure is distinctly subnormal in most models studied. Instead, filtration failure appears best attributed to intrarenal hemodynamic alterations. While certain facts tend to incriminate the renin-angiotensin system as the cause of the hemodynamic aberrations, others argue to the contrary. The issue is underactive investigation. (+info)

Renal function tests: what do they mean? A review of renal anatomy, biochemistry, and physiology. (2/6121)

Renal physiology, biochemistry, and anatomy are reviewed. For the most part, those aspects of these disciplines will be discussed which relate directly to the question of the evaluation of nephrotoxicity. In addition, emphasis is placed on those procedures and techniques which are useful in the evaluation of nephrotoxicity. A detailed discussion of histological and anatomical considerations is not given, since this is probably the least useful criterion for evaluation of renal damage. This information is intended as background for the remainder of the symposium which will be directed toward an understanding of specific nephrotoxicity phenomena. (+info)

NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. (3/6121)

In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity. (+info)

Recovery following relief of unilateral ureteral obstruction in the neonatal rat. (4/6121)

BACKGROUND: Obstructive nephropathy is a primary cause of renal insufficiency in infants and children. This study was designed to distinguish the reversible and irreversible cellular consequences of temporary unilateral ureteral obstruction (UUO) on the developing kidney. METHODS: Rats were subjected to UUO or sham operation in the first 48 hours of life, and the obstruction was removed five days later (or was left in place). Kidneys were removed for study 14 or 28 days later. In additional groups, kidneys were removed at the end of five days of obstruction. Immunoreactive distribution of renin was determined in arterioles, and the distribution of epidermal growth factor, transforming growth factor-beta1, clusterin, vimentin, and alpha-smooth muscle actin was determined in tubules and/or interstitium. The number of glomeruli, glomerular maturation, tubular atrophy, and interstitial collagen deposition was determined by morphometry. Renal cellular proliferation and apoptosis were measured by proliferating cell nuclear antigen and the TdT uridine-nick-end-label technique, respectively. The glomerular filtration rate was measured by inulin clearance. RESULTS: Renal microvascular renin maintained a fetal distribution with persistent UUO; this was partially reversed by the relief of obstruction. Although glomerular maturation was also delayed and glomerular volume was reduced by UUO, the relief of obstruction prevented the reduction in glomerular volume. Although relief of obstruction did not reverse a 40% reduction in the number of nephrons, the glomerular filtration rate of the postobstructed kidney was normal. The relief of obstruction did not improve tubular cell proliferation and only partially reduced apoptosis induced by UUO. This was associated with a persistent reduction in the tubular epidermal growth factor. In addition, the relief of obstruction reduced but did not normalize tubular expression of transforming growth factor-beta1, clusterin, and vimentin, all of which are evidence of persistent tubular injury. The relief of obstruction significantly reduced interstitial fibrosis and expression of alpha-smooth muscle actin by interstitial fibroblasts, but not to normal levels. CONCLUSIONS: The relief of obstruction in the neonatal rat attenuates, but does not reverse, renal vascular, glomerular, tubular, and interstitial injury resulting from five days of UUO. Hyperfiltration by remaining nephrons and residual tubulointerstitial injury in the postobstructed kidney are likely to lead to deterioration of renal function later in life. (+info)

Plasma total homocysteine and cysteine in relation to glomerular filtration rate in diabetes mellitus. (5/6121)

BACKGROUND: The plasma concentrations of total homocysteine (tHcy) and total cysteine (tCys) are determined by intracellular metabolism and by renal plasma clearance, and we hypothesized that glomerular filtration is a major determinant of plasma tHcy and tCys. We studied the relationships between the glomerular filtration rate (GFR) and plasma tHcy and tCys in populations of diabetic patients with particularly wide ranges of GFR. METHODS: We measured GFR, urine albumin excretion rate (UAER), plasma tHcy, tCys, methionine, vitamin B12, folate, C-peptide, and routine parameters in 50 insulin-dependent diabetes mellitus (IDDM) and 30 non-insulin-dependent diabetes mellitus (NIDDM) patients. All patients underwent intensive insulin treatment and had a serum creatinine concentration below 115 micromol/liter. RESULTS: Mean plasma tHcy in diabetic patients (0.1 micromol/liter) was lower than in normal persons (11.1 micromol/liter, P = 0.0014). Mean plasma tCys in diabetic patients (266.1 micromol/liter) was also lower than in normal persons (281.9 micromol/liter, P = 0.0005). Seventy-three percent of the diabetic patients had relative hyperfiltration. Plasma tHcy and tCys were closely and independently associated with GFR, serum folate, and serum B12. However, plasma tHcy was not independently associated with any of the 22 other variables tested, including age, serum creatinine concentration, UAER, total daily insulin dose, and glycemic control. CONCLUSIONS: Glomerular filtration rate is an independent determinant of plasma tHcy and tCys concentrations, and GFR is rate limiting for renal clearance of both homocysteine and cysteine in diabetic patients without overt nephropathy. Declining GFR explains the age-related increase in plasma tHcy, and hyperfiltration explains the lower than normal mean plasma tHcy and tCys concentrations in populations of diabetic patients. (+info)

Acute haemodynamic and proteinuric effects of prednisolone in patients with a nephrotic syndrome. (6/6121)

BACKGROUND: Administration of prednisolone causes an abrupt rise in proteinuria in patients with a nephrotic syndrome. METHODS: To clarify the mechanisms responsible for this increase in proteinuria we have performed a placebo controlled study in 26 patients with a nephrotic syndrome. Systemic and renal haemodynamics and urinary protein excretion were measured after prednisolone and after placebo. RESULTS: After i.v. administration of 125-150 mg prednisolone total proteinuria increased from 6.66+/-4.42 to 9.37+/-6.07 mg/min (P<0.001). By analysing the excretion of proteins with different charge and weight (albumin, transferrin, IgG, IgG4 and beta2-microglobulin) it became apparent that the increase of proteinuria was the result of a change in size selectivity rather than a change in glomerular charge selectivity or tubular protein reabsorption. Glomerular filtration rate rose from 83+/-34 ml to 95+/-43 ml/min (P<0.001) after 5 h, whereas effective renal plasma flow and endogenous creatinine clearance remained unchanged. As a result filtration fraction was increased, compatible with an increased glomerular pressure, which probably contributes to the size selectivity changes. Since corticosteroids affect both the renin-angiotensin system and renal prostaglandins, we have evaluated the effects of prednisolone on proteinuria after pretreatment with 3 months of the angiotensin-converting enzyme inhibitor lisinopril or after 2 weeks of the prostaglandin synthesis inhibitor indomethacin. Neither drug had any effect on prednisolone-induced increases of proteinuria. CONCLUSIONS: Prednisolone increases proteinuria by changing the size selective barrier of the glomerular capillary. Neither the renin-angiotensin axis nor prostaglandins seem to be involved in these effects of prednisolone on proteinuria. (+info)

Antiproteinuric efficacy of verapamil in comparison to trandolapril in non-diabetic renal disease. (7/6121)

BACKGROUND: Non-dihydropyridine calcium antagonists such as verapamil are equally effective in reducing proteinuria as ACE inhibitors in hypertensive patients with diabetic nephropathy. To date it is unknown whether verapamil elucidates such an antiproteinuric capacity in non-diabetic renal disease. METHODS: We performed a double-blind, placebo-controlled, random cross-over study which compared the antiproteinuric effect of 6 weeks treatment with verapamil SR (360 mg) to that of the ACE inhibitor trandolapril (4 mg), and their fixed combination vera/tran (180 mg verapamil SR and 2 mg trandolapril) in 11 non-diabetic patients with proteinuria of 6.6 (5.1-8.8) g/day, a creatinine clearance of 87 (74-106) ml/min, and a 24-h blood pressure of 136/85 (126/76-157/96) mmHg at baseline. RESULTS: Twenty-four-hour mean arterial pressure did not change during verapamil, whereas both trandolapril and vera/tran induced a significant reduction in MAP. Verapamil showed no significant effects on renal haemodynamics. Trandolapril and vera/tran did not significantly change GFR, but ERPF increased and FF decreased during both treatments (P<0.05). The antiproteinuric response of verapamil was significantly less compared to that of trandolapril and vera/tran (-12% (-17/-1) vs -51% (-56/-25) and -41% (-50/-19) respectively). The blood pressure and antiproteinuric response during verapamil tended to be greater in hypertensive patients than in normotensive patients, although this difference was not significant. Baseline blood pressure was related to the change in blood pressure during verapamil (r = -0.70; P < 0.02). CONCLUSIONS: The antiproteinuric and antihypertensive response of verapamil is less than that of the ACE inhibitor trandolapril in patients with non-diabetic renal disease. In contrast to the antiproteinuric response of trandolapril, the antiproteinuric reponse of verapamil seems to be completely dependent from effective blood pressure reduction. The fixed combination of verapamil and ACE inhibition at half doses has similar effects as ACE inhibition at full dose. (+info)

Hyperhomocyst(e)inaemia in children with chronic renal failure. (8/6121)

BACKGROUND: Hyperhomocyst(e)inaemia has been identified as a significant risk factor for the occurrence of atherosclerosis in adults with chronic renal failure. Because of its presumed direct toxic effect on the vascular wall, long-standing hyperhomocyst(e)inaemia in children with chronic renal failure might have an important influence on their risk of future development of atherosclerosis. Hitherto no data on hyperhomocyst(e)inaemia in children with renal failure have been published. METHODS: We investigated 16 children with chronic renal failure on conservative management, 12 children on haemodialysis and 17 children with a renal transplant. Age-matched controls were used for comparison. Plasma homocyst(e)ine levels after an overnight fast were determined by HPLC. Glomerular filtration rate was estimated by the Schwartz formula. RESULTS: Mean plasma homocyst(e)ine levels were 12.6 +/- 5.2 micromol/l in the conservatively managed group, 22.2 +/- 13.5 micromol/l in the haemodialysed group, 14.2 +/- 2.1 micromol/l in transplanted children with an estimated GFR > 60 ml/min/1.73 m2 and 17.5 +/- 5.1 micromol/l in transplanted children with a lower estimated GFR. In all groups homocyst(e)ine levels were significantly elevated as compared to controls. Homocyst(e)ine levels were significantly correlated with age and negatively correlated with estimated GFR and serum folate levels. CONCLUSIONS: Hyperhomocyst(e)inaemia is a feature of chronic renal failure in children as well as in adults. Elevated homocyst(e)ine levels can already be demonstrated in children with renal failure before end-stage renal disease has developed and persist after renal transplantation. Whether treatment of hyperhomocyst(e)inaemia in children with renal failure decreases the risk for future atherosclerosis remains to be proven. (+info)

Types of Kidney Diseases:

1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.

Symptoms of Kidney Diseases:

1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss

Diagnosis of Kidney Diseases:

1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)

Treatment of Kidney Diseases:

1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)

Prevention of Kidney Diseases:

1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings

Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.

The symptoms of chronic renal insufficiency can be subtle and may develop gradually over time. They may include fatigue, weakness, swelling in the legs and ankles, nausea, vomiting, and difficulty concentrating. As the disease progresses, patients may experience shortness of breath, heart failure, and peripheral artery disease.

Chronic renal insufficiency is diagnosed through blood tests that measure the level of waste products in the blood, such as creatinine and urea. Imaging studies, such as ultrasound and CT scans, may also be used to evaluate the kidneys and detect any damage or scarring.

Treatment for chronic renal insufficiency focuses on slowing the progression of the disease and managing its symptoms. This may include medications to control high blood pressure, diabetes, and anemia, as well as dietary changes and fluid restrictions. In severe cases, dialysis or kidney transplantation may be necessary.

Prevention of chronic renal insufficiency involves managing underlying conditions such as diabetes and hypertension, maintaining a healthy diet and exercise routine, and avoiding substances that can damage the kidneys, such as tobacco and excessive alcohol consumption. Early detection and treatment of kidney disease can help prevent the progression to chronic renal insufficiency.

Albuminuria is often associated with conditions such as diabetes, high blood pressure, and kidney disease, as these conditions can damage the kidneys and cause albumin to leak into the urine. It is also a common finding in people with chronic kidney disease (CKD), as the damaged kidneys are unable to filter out the excess protein.

If left untreated, albuminuria can lead to complications such as kidney failure, cardiovascular disease, and an increased risk of death. Treatment options for albuminuria include medications to lower blood pressure and control blood sugar levels, as well as dietary changes and lifestyle modifications. In severe cases, dialysis or kidney transplantation may be necessary.

In summary, albuminuria is the presence of albumin in the urine, which can be an indicator of kidney damage or disease. It is often associated with conditions such as diabetes and high blood pressure, and can lead to complications if left untreated.

A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).

Prevalence:

Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.

Causes:

The causes of chronic kidney failure are numerous and include:

1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.

Symptoms:

Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:

1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.

Diagnosis:

Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:

1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.

Imaging studies may include:

1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.

Treatment:

Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:

1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.

Complications:

Chronic kidney failure can lead to several complications, including:

1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.

Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.

Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.

There are two main types of Renal Insufficiency:

1. Acute Kidney Injury (AKI): This is a sudden and reversible decrease in kidney function, often caused by injury, sepsis, or medication toxicity. AKI can resolve with appropriate treatment and supportive care.
2. Chronic Renal Insufficiency (CRI): This is a long-standing and irreversible decline in kidney function, often caused by diabetes, high blood pressure, or chronic kidney disease. CRI can lead to ESRD if left untreated.

Signs and symptoms of Renal Insufficiency may include:

* Decreased urine output
* Swelling in the legs and ankles (edema)
* Fatigue
* Nausea and vomiting
* Shortness of breath (dyspnea)
* Pain in the back, flank, or abdomen

Diagnosis of Renal Insufficiency is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include urinalysis, blood urea nitrogen (BUN) and creatinine levels, and a 24-hour urine protein collection. Imaging studies, such as ultrasound or CT scans, may be used to evaluate the kidneys and rule out other possible causes of the patient's symptoms.

Treatment of Renal Insufficiency depends on the underlying cause and the severity of the condition. Treatment may include medications to control blood pressure, manage fluid balance, and reduce proteinuria (excess protein in the urine). In some cases, dialysis or a kidney transplant may be necessary.

Prevention of Renal Insufficiency includes managing underlying conditions such as diabetes and hypertension, avoiding nephrotoxic medications and substances, and maintaining a healthy diet and lifestyle. Early detection and treatment of acute kidney injury can also help prevent the development of chronic renal insufficiency.

In conclusion, Renal Insufficiency is a common condition that can have significant consequences if left untreated. It is important for healthcare providers to be aware of the causes, symptoms, and diagnosis of Renal Insufficiency, as well as the treatment and prevention strategies available. With appropriate management, many patients with Renal Insufficiency can recover and maintain their kidney function over time.

There are several types of diabetic nephropathy, including:

1. Mesangial proliferative glomerulonephritis: This is the most common type of diabetic nephropathy and is characterized by an overgrowth of cells in the mesangium, a part of the glomerulus (the blood-filtering unit of the kidney).
2. Segmental sclerosis: This type of diabetic nephropathy involves the hardening of some parts of the glomeruli, leading to decreased kidney function.
3. Fibrotic glomerulopathy: This is a rare form of diabetic nephropathy that is characterized by the accumulation of fibrotic tissue in the glomeruli.
4. Membranous nephropathy: This type of diabetic nephropathy involves the deposition of immune complexes (antigen-antibody complexes) in the glomeruli, leading to inflammation and damage to the kidneys.
5. Minimal change disease: This is a rare form of diabetic nephropathy that is characterized by minimal changes in the glomeruli, but with significant loss of kidney function.

The symptoms of diabetic nephropathy can be non-specific and may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Diagnosis is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies such as ultrasound or CT scans.

Treatment for diabetic nephropathy typically involves managing blood sugar levels through lifestyle changes (such as diet and exercise) and medication, as well as controlling high blood pressure and other underlying conditions. In severe cases, dialysis or kidney transplantation may be necessary. Early detection and management of diabetic nephropathy can help slow the progression of the disease and improve outcomes for patients with this condition.

The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.

There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.

Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

Renal artery obstruction can be caused by a variety of factors, including:

1. Atherosclerosis (hardening of the arteries): This is the most common cause of renal artery obstruction and occurs when plaque builds up in the arteries, leading to narrowing or blockages.
2. Stenosis (narrowing of the arteries): This can be caused by inflammation or scarring of the arteries, which can lead to a decrease in blood flow to the kidneys.
3. Fibromuscular dysplasia: This is a rare condition that causes abnormal growth of muscle tissue in the renal arteries, leading to narrowing or blockages.
4. Embolism (blood clot): A blood clot can break loose and travel to the kidneys, causing a blockage in the renal artery.
5. Renal vein thrombosis: This is a blockage of the veins that drain blood from the kidneys, which can lead to decreased blood flow and oxygenation of the kidneys.

Symptoms of renal artery obstruction may include:

1. High blood pressure
2. Decreased kidney function
3. Swelling in the legs or feet
4. Pain in the flank or back
5. Fatigue
6. Nausea and vomiting
7. Weight loss

Diagnosis of renal artery obstruction is typically made through a combination of physical examination, medical history, and diagnostic tests such as:

1. Ultrasound: This can help identify any blockages or narrowing in the renal arteries.
2. Computed tomography (CT) scan: This can provide detailed images of the renal arteries and any blockages or narrowing.
3. Magnetic resonance angiogram (MRA): This is a non-invasive test that uses magnetic fields and radio waves to create detailed images of the renal arteries.
4. Angiography: This is a minimally invasive test that involves inserting a catheter into the renal artery to visualize any blockages or narrowing.

Treatment for renal artery obstruction depends on the underlying cause and severity of the condition. Some possible treatment options include:

1. Medications: Drugs such as blood thinners, blood pressure medication, and anticoagulants may be prescribed to manage symptoms and slow the progression of the disease.
2. Endovascular therapy: This is a minimally invasive procedure in which a catheter is inserted into the renal artery to open up any blockages or narrowing.
3. Surgery: In some cases, surgery may be necessary to remove any blockages or repair any damage to the renal arteries.
4. Dialysis: This is a procedure in which waste products are removed from the blood when the kidneys are no longer able to do so.
5. Kidney transplantation: In severe cases of renal artery obstruction, a kidney transplant may be necessary.

It is important to note that early detection and treatment of renal artery obstruction can help prevent complications and improve outcomes for patients.

A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.

Note: Renal hypertension is also known as renal artery hypertension.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

Nephrosclerosis can be caused by a variety of factors, including:

1. Diabetes: High blood sugar levels over an extended period can damage the kidney tissues and lead to nephrosclerosis.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the kidney blood vessels, leading to scarring and hardening of the tissues.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood, can lead to nephrosclerosis.
4. Obesity: Excess weight can increase the risk of developing diabetes and hypertension, both of which are leading causes of nephrosclerosis.
5. Family history: A family history of kidney disease increases the risk of developing nephrosclerosis.
6. Certain medications: Long-term use of certain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain antibiotics can damage the kidneys and lead to nephrosclerosis.
7. Infections: Certain infections, such as pyelonephritis, can spread to the kidneys and cause inflammation and scarring that leads to nephrosclerosis.
8. Kidney stones: Recurring kidney stones can cause chronic inflammation and damage to the kidney tissues, leading to nephrosclerosis.
9. Certain medical conditions: Certain medical conditions, such as systemic lupus erythematosus and vasculitis, can increase the risk of developing nephrosclerosis.

Symptoms of nephrosclerosis may include:

1. Proteinuria: Excess protein in the urine.
2. Hematuria: Blood in the urine.
3. Reduced kidney function: Decreased ability of the kidneys to filter waste and excess fluids from the blood.
4. High blood pressure: Hypertension is common in people with nephrosclerosis.
5. Swelling: Fluid retention in the legs, ankles, and feet.
6. Fatigue: Weakness and tiredness due to the buildup of waste products in the body.
7. Nausea and vomiting: Due to the buildup of waste products in the body.
8. Skin rash: Some people with nephrosclerosis may develop a skin rash.

Nephrosclerosis can be diagnosed through a combination of physical examination, medical history, urine and blood tests, and imaging studies such as ultrasound and CT scans. Treatment for nephrosclerosis depends on the underlying cause and may include medications to control high blood pressure, reduce proteinuria, and slow the progression of the disease. In severe cases, dialysis or kidney transplantation may be necessary.

It is essential to seek medical attention if you experience any symptoms of nephrosclerosis, as early diagnosis and treatment can help prevent complications and improve outcomes. A healthcare professional can perform a physical examination, take a medical history, and order diagnostic tests to determine the underlying cause of your symptoms. Based on the severity and underlying cause of your condition, a treatment plan will be developed that may include medications, lifestyle modifications, or dialysis. With proper treatment, many people with nephrosclerosis can manage their symptoms and improve their quality of life.

Symptoms of renovascular hypertension may include:

* High blood pressure that is resistant to treatment
* Flank pain or back pain
* Hematuria (blood in the urine)
* Proteinuria (excess protein in the urine)
* Decreased kidney function

Diagnosis of renovascular hypertension typically involves imaging tests such as angiography, CT or MRI angiography, or ultrasound to evaluate the renal arteries and identify any blockages or narrowing. Other tests such as arenography, captopril test, or adrenomedullin testing may also be used to support the diagnosis.

Treatment of renovascular hypertension typically involves medications to lower blood pressure, such as beta blockers, ACE inhibitors, or calcium channel blockers. In some cases, surgery may be necessary to restore blood flow to the kidneys. For example, atherosclerosis can be treated with angioplasty or bypass surgery.

It is important to note that renovascular hypertension is a relatively rare cause of hypertension and only accounts for about 5-10% of all cases of hypertension. However, it is an important differential diagnosis for hypertension that is resistant to treatment or has a sudden onset.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.

Key Features of Cardio-Renal Syndrome:

1. Cardiac dysfunction: CRS is characterized by impaired cardiac function, including decreased left ventricular ejection fraction, reduced cardiac output, and abnormal heart rhythms.
2. Renal dysfunction: The condition is associated with acute kidney injury (AKI) or chronic kidney disease (CKD), which can lead to fluid overload, electrolyte imbalance, and metabolic disturbances.
3. Vasoplegia: CRS is often accompanied by vasoplegia, a condition characterized by hypotension, low systemic vascular resistance, and impaired vasomotor tone.
4. Sepsis or shock: CRS frequently develops in patients with sepsis or shock, who have severe inflammation and organ dysfunction.
5. Multi-organ involvement: The syndrome can affect multiple organs, including the heart, kidneys, liver, and brain.

Pathophysiology of Cardio-Renal Syndrome:

The pathophysiology of CRS is complex and involves a series of interrelated events. Key mechanisms include:

1. Inflammation: Sepsis or shock triggers an inflammatory response, which can lead to cardiac and renal dysfunction.
2. Oxidative stress: Reactive oxygen species (ROS) can damage cardiac and renal tissues, contributing to the development of CRS.
3. Endothelial dysfunction: Impaired endothelial function can impair vasodilation and promote vasoconstriction, leading to hypertension or hypotension.
4. Neurohormonal activation: The hypothalamic-pituitary-adrenal (HPA) axis is activated, leading to the release of stress hormones such as cortisol and catecholamines.
5. Cardiac dysfunction: Sepsis-induced cardiomyopathy can lead to decreased cardiac output, impaired sodium-potassium pump function, and altered autonomic tone.
6. Renal dysfunction: Injury to the renal tissues can lead to decreased renal blood flow, increased proteinuria, and impaired urinary concentrating ability.

Diagnosis of Cardio-Renal Syndrome:

The diagnosis of CRS is based on a combination of clinical, laboratory, and imaging studies. Key diagnostic criteria include:

1. Clinical signs of hypotension or shock.
2. Laboratory evidence of inflammation (e.g., elevated white blood cell count, elevated serum creatinine).
3. Echocardiographic or other imaging studies demonstrating cardiac dysfunction.
4. Urinary output and sodium balance assessment to evaluate fluid status.
5. Measurement of plasma levels of natriuretic peptides (e.g., B-type natriuretic peptide, N-terminal pro-B-type natriuretic peptide) to assess cardiac function.
6. Assessment of renal function using serum creatinine and urinary protein levels.

Treatment of Cardio-Renal Syndrome:

The treatment of CRS is aimed at addressing the underlying causes of both cardiac and renal dysfunction. Key therapeutic strategies include:

1. Fluid management: Initiation of fluid resuscitation with crystalloids or colloids to restore blood volume and urine output, while avoiding excessive fluid administration that can exacerbate cardiac dysfunction and worsen renal impairment.
2. Vasoactive medications: Use of vasopressors to enhance systemic vascular resistance and improve cardiac function, while avoiding dopamine or other agents that can worsen renal function.
3. Diuretics: Administration of loop diuretics to promote urinary sodium and water excretion, which can help manage fluid overload and improve renal function.
4. Anti-inflammatory therapy: Use of corticosteroids or other anti-inflammatory agents to reduce inflammation and immune-mediated damage in the setting of acute kidney injury.
5. Nutritional support: Provision of adequate nutrition, including supplementation with essential vitamins and minerals, to promote recovery and minimize catabolism.
6. Monitoring and adjustment of medications: Regular monitoring of blood pressure, heart rate, and renal function, along with adjustments in medication dosages and types as needed to optimize therapeutic effects while avoiding adverse consequences.
7. Dialysis: Initiation of dialysis in cases of severe acute kidney injury or when other therapies are insufficient to maintain fluid-electrolyte balance and prevent complications.
8. Addressing underlying causes: Management of underlying conditions, such as sepsis, shock, or urinary obstruction, to help restore renal function and prevent recurrence of acute kidney injury.
9. Hemodialysis: Use of hemodialysis in cases of severe acute kidney injury or when other therapies are insufficient to maintain fluid-electrolyte balance and prevent complications.
10. Continuous renal replacement therapy (CRRT): Use of CRRT in cases of severe acute kidney injury or when other therapies are insufficient to maintain fluid-electrolyte balance and prevent complications.

It is important to note that the choice of therapy will depend on the underlying cause of acute kidney injury, the severity of the condition, and the patient's overall medical status and comorbidities.

There are two main types of heart failure:

1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.

Symptoms of heart failure may include:

* Shortness of breath
* Fatigue
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness

Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).

It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

GN IGA is one of the most common forms of idiopathic membranous nephropathy, which means it has no known cause. It can occur at any age but is more common in adults between the ages of 20 and 40. The disease often progresses slowly over several years, and some people may experience no symptoms at all.

The diagnosis of GN IGA is based on a combination of clinical findings, laboratory tests, and kidney biopsy. Laboratory tests may show abnormal levels of proteins in the urine, such as albumin, and a high level of IgA in the blood. A kidney biopsy is often necessary to confirm the diagnosis and to rule out other kidney diseases.

There is no cure for GN IGA, but treatment can help slow the progression of the disease. Treatment options may include medications to control high blood pressure, reduce proteinuria (excess protein in the urine), and suppress the immune system. In severe cases, dialysis or a kidney transplant may be necessary.

Preventive measures for GN IGA are not well established, but maintaining a healthy lifestyle, including a balanced diet, regular exercise, and avoiding exposure to toxins, may help reduce the risk of developing the disease. It is also important to manage any underlying medical conditions, such as high blood pressure or diabetes, which can increase the risk of kidney damage.

There are several possible causes of hyperuricemia, including:

* Overproduction of uric acid: This can occur due to a diet high in purines, certain medical conditions such as gout or leukemia, or certain medications such as aspirin and some antibiotics.
* Underactive thyroid (hypothyroidism): This can cause the body to produce more uric acid than usual.
* Kidney problems: If the kidneys are not functioning properly, they may not be able to remove excess uric acid from the blood, leading to hyperuricemia.
* Dehydration: When the body is dehydrated, it produces more uric acid as a way to conserve water.

Symptoms of hyperuricemia can include joint pain and inflammation, particularly in the big toe (gout), kidney stones, and a burning sensation while urinating. In some cases, hyperuricemia may not cause any symptoms at all.

Treatment for hyperuricemia depends on the underlying cause of the condition. Medications such as allopurinol or probenecid can be used to reduce uric acid production or improve its excretion. In some cases, changes to diet and lifestyle may also be recommended, such as avoiding foods high in purines, drinking plenty of water, and managing underlying medical conditions.

If left untreated, hyperuricemia can lead to complications such as kidney damage, gout attacks, and an increased risk of certain types of kidney stones. Therefore, it is important to seek medical attention if symptoms persist or worsen over time.

The term "segmental" refers to the fact that the scarring or hardening occurs in a specific segment of the glomerulus. Focal segmental glomerulosclerosis can be caused by a variety of factors, including diabetes, high blood pressure, and certain infections or injuries.

Symptoms of focal segmental glomerulosclerosis may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Treatment options vary depending on the underlying cause, but may include medications to control high blood pressure or diabetes, as well as immunosuppressive drugs in cases where the condition is caused by an autoimmune disorder. In severe cases, dialysis or kidney transplantation may be necessary.

Treatment for uremia typically involves dialysis or kidney transplantation to remove excess urea from the blood and restore normal kidney function. In some cases, medications may be prescribed to help manage symptoms such as high blood pressure, anemia, or electrolyte imbalances.

The term "uremia" is derived from the Greek words "oura," meaning "urea," and "emia," meaning "in the blood." It was first used in the medical literature in the late 19th century to describe a condition caused by excess urea in the blood. Today, it remains an important diagnostic term in nephrology and is often used interchangeably with the term "uremic syndrome."

Treatment for ureteral obstruction depends on the underlying cause and may include medications, endoscopic procedures, or surgery. In some cases, a temporary drainage catheter may be placed in the ureter to help relieve symptoms until the blockage can be fully treated.

Ureteral obstruction can be acute or chronic, and may occur in adults or children. It is important to seek medical attention if symptoms persist or worsen over time, as untreated ureteral obstruction can lead to complications such as kidney damage or sepsis.

Causes of Ureteral Obstruction:

Ureteral obstruction can be caused by a variety of factors, including:

1. Kidney stones: Small, hard mineral deposits that form in the urine and can block the flow of urine through the ureters.
2. Tumors: Cancerous or non-cancerous growths that can block the ureters.
3. Scar tissue: Scarring from previous surgeries or injuries can cause narrowing or blockages in the ureters.
4. Prostate enlargement: In men, an enlarged prostate gland can press on the urethra and ureters, causing blockages.
5. Bladder neck obstruction: A condition where the bladder neck is narrow or blocked, preventing urine from flowing through the urethra.
6. Trauma: Injuries to the ureters or bladder can cause blockages.
7. Inflammation: Inflammation in the ureters or kidneys can cause swelling and blockages.
8. Congenital conditions: Some people may be born with abnormalities that cause blockages in the urinary tract.
9. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, or spinal cord injuries can affect the nerves that control the bladder and ureters, leading to blockages.
10. Medications: Certain medications, such as certain antibiotics and chemotherapy drugs, can cause damage to the ureters and lead to blockages.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

Causes of Hyperkalemia:

1. Kidney dysfunction: When the kidneys are not able to excrete excess potassium, it can build up in the bloodstream and lead to hyperkalemia.
2. Medications: Certain drugs, such as ACE inhibitors, potassium-sparing diuretics, and NSAIDs, can increase potassium levels by blocking the excretion of potassium in the urine.
3. Diabetic ketoacidosis: High levels of potassium can occur in people with uncontrolled diabetes who have diabetic ketoacidosis.
4. Acute kidney injury: This condition can cause a rapid increase in potassium levels as the kidneys are unable to remove excess potassium from the blood.
5. Heart disease: Potassium levels can rise in people with heart failure or other cardiac conditions, leading to hyperkalemia.

Symptoms of Hyperkalemia:

1. Muscle weakness and fatigue
2. Abnormal heart rhythms (arrhythmias)
3. Palpitations
4. Constipation
5. Nausea and vomiting
6. Abdominal cramps
7. Fatigue
8. Confusion
9. Headaches
10. Weakness in the legs and feet

Treatment of Hyperkalemia:

The treatment of hyperkalemia depends on the underlying cause and the severity of the condition. Some of the common methods for lowering potassium levels include:

1. Diuretics: These medications help remove excess fluid and electrolytes, including potassium, from the body.
2. Calcium gluconate: This medication can help stabilize cardiac function and reduce the risk of arrhythmias.
3. Insulin and glucose: Giving insulin and glucose to someone with diabetic ketoacidosis can help lower potassium levels by increasing glucose uptake in the cells.
4. Hemodialysis: This is a process that uses a machine to filter waste products, including excess potassium, from the blood.
5. Potassium-binding resins: These medications can bind to potassium ions in the gut and prevent their absorption into the bloodstream.
6. Sodium polystyrene sulfonate (Kayexalate): This medication can help lower potassium levels by binding to excess potassium in the gut and causing it to be eliminated in the stool.
7. Activated charcoal: This medication can help bind to potassium ions in the gut and prevent their absorption into the bloodstream.

In severe cases of hyperkalemia, hospitalization may be necessary to monitor and treat the condition. In some instances, dialysis may be required to remove excess potassium from the blood. It is important to note that the treatment for hyperkalemia should only be done under the guidance of a healthcare professional, as some medications or procedures can worsen the condition if not properly managed.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:

1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.

The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.

Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.

Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.

In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.

There are several types of alkalosis, including:

1. Respiratory alkalosis: This type is caused by an excessive breathing of carbon dioxide into the lungs, which increases the bicarbonate levels in the blood.
2. Metabolic alkalosis: This type is caused by a decrease in the production of acid in the body, such as in diabetic ketoacidosis or liver disease.
3. Inherited alkalosis: This type is caused by inherited genetic disorders that affect the regulation of acid-base homeostasis.
4. Drug-induced alkalosis: Certain medications, such as antacids and diuretics, can increase bicarbonate levels in the blood.
5. Post-operative alkalosis: This type can occur after surgery, particularly gastrointestinal surgery, due to the release of bicarbonate from damaged tissues.

The symptoms of alkalosis can vary depending on the severity and duration of the condition. They may include:

* Nausea and vomiting
* Abdominal pain
* Headache
* Fatigue
* Muscle weakness
* Tingling sensations in the extremities
* Confusion and disorientation

If left untreated, alkalosis can lead to more severe complications such as:

* Respiratory acidosis (a decrease in blood pH due to a lack of oxygen)
* Cardiac arrhythmias (irregular heartbeats)
* Seizures
* Coma

Diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Laboratory tests may include:

* Arterial blood gas (ABG) analysis to measure the pH and PCO2 levels in the blood
* Serum electrolyte levels to assess the levels of sodium, potassium, and chloride
* Urine testing to assess the levels of bicarbonate and other electrolytes

Treatment of alkalosis depends on the underlying cause and severity of the condition. General measures may include:

* Correction of any underlying metabolic disorders, such as diabetes or kidney disease
* Discontinuation of medications that may be contributing to the alkalosis
* Fluid and electrolyte replacement to correct dehydration or imbalances
* Oxygen therapy to treat respiratory acidosis

In severe cases, hospitalization may be necessary to monitor and treat the condition. In some cases, medications such as sodium bicarbonate may be prescribed to help restore acid-base balance. Surgery may be required in cases where the alkalosis is caused by a structural problem, such as a hiatal hernia.

Prognosis for alkalosis depends on the underlying cause and severity of the condition. In general, early diagnosis and treatment can improve outcomes. However, untreated severe alkalosis can lead to complications such as seizures, coma, and cardiac arrhythmias.

Prevention of alkalosis involves identifying and treating underlying conditions that may contribute to the development of the condition. This includes managing chronic diseases such as diabetes and kidney disease, and avoiding medications that may cause alkalosis. Additionally, maintaining a balanced diet and staying hydrated can help prevent electrolyte imbalances that can lead to alkalosis.

In conclusion, alkalosis is a condition characterized by an excess of base in the body, which can lead to respiratory and metabolic disturbances. The diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Treatment depends on the underlying cause and severity of the condition, and may include fluid and electrolyte replacement, medication, and addressing any underlying conditions. Early diagnosis and treatment can improve outcomes for patients with alkalosis.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Anuria is often associated with other conditions such as chronic kidney disease, sepsis, or bladder outlet obstruction. The symptoms of anuria may include decreased urine output, swelling in the legs and abdomen, nausea, vomiting, and electrolyte imbalances.

Treatment of anuria depends on the underlying cause, and may involve medications to relieve symptoms, drainage of obstructions, or other interventions such as hemodialysis or peritoneal dialysis. In severe cases, anuria can lead to uremia, a buildup of waste products in the blood that can be life-threatening. Therefore, prompt medical attention is essential for effective management and prevention of complications.

1. Heart Disease: High blood sugar levels can damage the blood vessels and increase the risk of heart disease, which includes conditions like heart attacks, strokes, and peripheral artery disease.
2. Kidney Damage: Uncontrolled diabetes can damage the kidneys over time, leading to chronic kidney disease and potentially even kidney failure.
3. Nerve Damage: High blood sugar levels can damage the nerves in the body, causing numbness, tingling, and pain in the hands and feet. This is known as diabetic neuropathy.
4. Eye Problems: Diabetes can cause changes in the blood vessels of the eyes, leading to vision problems and even blindness. This is known as diabetic retinopathy.
5. Infections: People with diabetes are more prone to developing skin infections, urinary tract infections, and other types of infections due to their weakened immune system.
6. Amputations: Poor blood flow and nerve damage can lead to amputations of the feet or legs if left untreated.
7. Cognitive Decline: Diabetes has been linked to an increased risk of cognitive decline and dementia.
8. Sexual Dysfunction: Men with diabetes may experience erectile dysfunction, while women with diabetes may experience decreased sexual desire and vaginal dryness.
9. Gum Disease: People with diabetes are more prone to developing gum disease and other oral health problems due to their increased risk of infection.
10. Flu and Pneumonia: Diabetes can weaken the immune system, making it easier to catch the flu and pneumonia.

It is important for people with diabetes to manage their condition properly to prevent or delay these complications from occurring. This includes monitoring blood sugar levels regularly, taking medication as prescribed by a doctor, and following a healthy diet and exercise plan. Regular check-ups with a healthcare provider can also help identify any potential complications early on and prevent them from becoming more serious.

The exact cause of NFD is not fully understood, but it is believed to be related to the buildup of a protein called amyloid in the skin. This buildup leads to inflammation and the deposition of abnormal fibers in the dermis, which causes the skin to thicken and become rigid.

The symptoms of NFD can vary in severity and may include:

1. Thickening and hardening of the skin, particularly on the legs, arms, and torso
2. Limited joint mobility
3. Pain or discomfort in the affected areas
4. Difficulty with everyday activities such as walking, dressing, or bathing
5. Skin tightness and itchiness

There is no cure for NFD, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These may include:

1. Topical creams and ointments to reduce itching and inflammation
2. Physical therapy to maintain joint mobility and strength
3. Pain management medications
4. Surgery to remove excess skin tissue
5. Dialysis-related treatments to address underlying kidney disease

It is important for individuals with NFD to work closely with their healthcare team to develop a comprehensive treatment plan that addresses their specific needs and helps manage their symptoms. With appropriate care, individuals with NFD can improve their quality of life and maintain their independence.

A type of inflammatory kidney disease that affects the interstitial tissue surrounding the tubules of the kidney. It is characterized by inflammation and fibrosis (scarring) of the interstitium, leading to impaired kidney function. The exact cause of interstitial nephritis is not always known, but it can be triggered by a variety of factors, including infections, allergic reactions, and certain medications. Symptoms may include fever, joint pain, and loss of appetite, and the condition can progress to end-stage renal disease if left untreated. Treatment typically involves medication to reduce inflammation and manage symptoms, as well as supportive care to help the kidneys function properly.

There are several types of hypertrophy, including:

1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).

Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.

In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.

There are many potential causes of dehydration, including:

* Not drinking enough fluids
* Diarrhea or vomiting
* Sweating excessively
* Diabetes (when the body cannot properly regulate blood sugar levels)
* Certain medications
* Poor nutrition
* Infections
* Poor sleep

To diagnose dehydration, a healthcare provider will typically perform a physical examination and ask questions about the patient's symptoms and medical history. They may also order blood tests or other diagnostic tests to rule out other conditions that may be causing the symptoms.

Treatment for dehydration usually involves drinking plenty of fluids, such as water or electrolyte-rich drinks like sports drinks. In severe cases, intravenous fluids may be necessary. If the underlying cause of the dehydration is a medical condition, such as diabetes or an infection, treatment will focus on managing that condition.

Preventing dehydration is important for maintaining good health. This can be done by:

* Drinking enough fluids throughout the day
* Avoiding caffeine and alcohol, which can act as diuretics and increase urine production
* Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains
* Avoiding excessive sweating by dressing appropriately for the weather and taking breaks in cool, shaded areas when necessary
* Managing medical conditions like diabetes and kidney disease properly.

In severe cases of dehydration, complications can include seizures, organ failure, and even death. It is important to seek medical attention if symptoms persist or worsen over time.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

In addition to the high blood pressure, people with malignant hypertension may experience other signs and symptoms, such as:

* Seizures or coma
* Vision changes or loss of vision
* Numbness or weakness in the face, arm, or leg
* Confusion or disorientation
* Slurred speech
* Difficulty speaking or swallowing
* Severe headache
* Neck stiffness
* Fever
* Pain in the chest, abdomen, or flank

If left untreated, malignant hypertension can lead to a range of complications and organ damage, including:

* Heart attack or heart failure
* Stroke or cerebral hemorrhage
* Kidney failure or renal impairment
* Seizures or coma
* Vision loss or blindness
* Peripheral artery disease or limb gangrene

Treatment of malignant hypertension typically involves aggressive medication to lower blood pressure and manage symptoms, as well as careful monitoring in a hospital setting. In severe cases, surgery or other interventions may be necessary to treat underlying conditions or repair damaged organs. With prompt and appropriate treatment, the outlook for people with malignant hypertension can improve significantly, but delays in diagnosis and treatment can have serious consequences.

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There are several types of RTA, including:

1. Type 1 RTA: This is caused by a defect in the genes that code for the proteins involved in acid secretion in the renal tubules.
2. Type 2 RTA: This is caused by damage to the renal tubules, such as from exposure to certain drugs or toxins.
3. Type 4 RTA: This is caused by a deficiency of the hormone aldosterone, which helps regulate electrolyte levels in the body.

Symptoms of RTA can include:

* Nausea and vomiting
* Abdominal pain
* Fatigue
* Weakness
* Dehydration
* Increased heart rate
* Decreased urine production

RTA can be diagnosed through blood tests that measure the pH levels in the body, as well as tests that assess kidney function and electrolyte levels. Treatment for RTA typically involves correcting any underlying causes, such as stopping certain medications or addressing electrolyte imbalances. In some cases, medications may be prescribed to help regulate acid levels in the body.

Prevention of RTA includes maintaining proper hydration, avoiding exposure to harmful substances, and managing any underlying medical conditions that may increase the risk of developing RTA. Early detection and treatment can help prevent complications and improve outcomes for individuals with RTA.

The primary cause of systolic heart failure is typically related to damage or disease affecting the left ventricle, such as coronary artery disease, hypertension, or cardiomyopathy. Other contributing factors may include valvular heart disease, anemia, and thyroid disorders.

Diagnosis of systolic heart failure often involves a physical examination, medical history, and diagnostic tests such as electrocardiography (ECG), echocardiography, and blood tests. Treatment options for systolic heart failure may include lifestyle modifications, medications to manage symptoms and slow progression of the disease, and in severe cases, implantable devices or surgical interventions such as left ventricular assist devices (LVADs) or heart transplantation.

Systolic heart failure is a serious medical condition that can significantly impact quality of life and longevity if left untreated or undertreated. Therefore, early diagnosis and aggressive management are essential to improve outcomes for patients with this condition.

Nephritis is often diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis and blood tests. Treatment for nephritis depends on the underlying cause, but may include antibiotics, corticosteroids, and immunosuppressive medications. In severe cases, dialysis may be necessary to remove waste products from the blood.

Some common types of nephritis include:

1. Acute pyelonephritis: This is a type of bacterial infection that affects the kidneys and can cause sudden and severe symptoms.
2. Chronic pyelonephritis: This is a type of inflammation that occurs over a longer period of time, often as a result of recurrent infections or other underlying conditions.
3. Lupus nephritis: This is a type of inflammation that occurs in people with systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple organs.
4. IgA nephropathy: This is a type of inflammation that occurs when an antibody called immunoglobulin A (IgA) deposits in the kidneys and causes damage.
5. Mesangial proliferative glomerulonephritis: This is a type of inflammation that affects the mesangium, a layer of tissue in the kidney that helps to filter waste products from the blood.
6. Minimal change disease: This is a type of nephrotic syndrome (a group of symptoms that include proteinuria, or excess protein in the urine) that is caused by inflammation and changes in the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
7. Membranous nephropathy: This is a type of inflammation that occurs when there is an abnormal buildup of antibodies called immunoglobulin G (IgG) in the glomeruli, leading to damage to the kidneys.
8. Focal segmental glomerulosclerosis: This is a type of inflammation that affects one or more segments of the glomeruli, leading to scarring and loss of function.
9. Post-infectious glomerulonephritis: This is a type of inflammation that occurs after an infection, such as streptococcal infections, and can cause damage to the kidneys.
10. Acute tubular necrosis (ATN): This is a type of inflammation that occurs when there is a sudden loss of blood flow to the kidneys, causing damage to the tubules, which are tiny tubes in the kidneys that help to filter waste products from the blood.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

VUR occurs when the muscles in the ureteral walls are weak or underdeveloped, allowing urine to flow back into the bladder instead of emptying properly into the ureters. It can also be caused by an abnormal connection between the bladder and the ureter, such as a birth defect or injury.

Symptoms of VUR may include recurring UTIs, fever, painful urination, and blood in the urine. To diagnose VUR, doctors may use imaging tests such as ultrasound or renal scan to visualize the flow of urine.

Treatment for VUR depends on the severity of the condition and may include antibiotics to treat UTIs, medication to relax the bladder muscle, and in some cases, surgery to repair any abnormal connections or narrowing of the ureters.

The symptoms of Fanconi Syndrome can vary in severity and may include:

* Diarrhea
* Dehydration
* Abdominal pain
* Failure to gain weight or grow at the expected rate
* Increased risk of infections
* Poor blood sugar control
* High levels of amino acids in the urine
* Abnormal kidney function

Fanconi Syndrome is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the condition typically involves managing the symptoms and addressing any underlying complications. This may include:

* Nutritional support to ensure adequate intake of essential nutrients
* Hydration to prevent dehydration
* Antibiotics to prevent or treat infections
* Medications to manage diarrhea and abdominal pain
* Monitoring of blood sugar levels
* Kidney function tests to monitor for any kidney damage

There is no cure for Fanconi Syndrome, but with proper management, individuals with the condition can lead relatively normal lives. It is important for individuals with Fanconi Syndrome to receive regular medical care and follow a carefully planned diet to manage their symptoms and prevent complications.

There are several types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.

It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.

Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.

There are many different types of fibrosis, including:

* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.

Fibrosis can be diagnosed through a variety of methods, including:

* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.

There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:

* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.

It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.

Symptoms of AAN include:

1. Proteinuria (excess protein in the urine)
2. Hematuria (blood in the urine)
3. Reduced kidney function
4. Swelling in the legs and ankles
5. Fatigue
6. Weight loss

Causes and risk factors:

1. HIV infection
2. Chronic immune activation and inflammation
3. High blood pressure
4. Diabetes mellitus
5. Obesity

Diagnosis:

1. Urine test for protein and blood
2. Kidney function tests (estimated glomerular filtration rate)
3. Biopsy of the kidney to examine for inflammation and scarring

Treatment:

1. Antiretroviral therapy (ART) to control HIV infection
2. Blood pressure-lowering medications
3. Medications to control proteinuria (e.g., angiotensin-converting enzyme inhibitors or angiotensin receptor blockers)
4. Medications to reduce inflammation and slow progression of the disease (e.g., corticosteroids or immunosuppressive drugs)
5. Dialysis or kidney transplant for advanced ESRD

Prognosis:

The prognosis for AAN is generally poor, with a high risk of progression to ESRD and mortality. However, early detection and treatment can improve outcomes. It is essential for individuals living with HIV/AIDS to receive regular monitoring and screening for kidney disease to prevent or delay the progression of AAN.

The symptoms of pyelonephritis can vary depending on the severity and location of the infection, but may include:

* Fever
* Chills
* Flank pain (pain in the sides or back)
* Nausea and vomiting
* Frequent urination or difficulty urinating
* Blood in the urine
* Abdominal tenderness
* Loss of appetite

Pyelonephritis can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis, blood cultures, and imaging studies (such as CT or ultrasound scans).

Treatment of pyelonephritis typically involves antibiotics to eradicate the underlying bacterial infection, as well as supportive care to manage symptoms such as fever and pain. In severe cases, hospitalization may be necessary to monitor and treat the infection.

If left untreated, pyelonephritis can lead to serious complications such as kidney damage, sepsis, and even death. Therefore, prompt recognition and treatment of this condition are crucial to prevent long-term consequences and improve outcomes for affected individuals.

In diabetes, polyuria is caused by high levels of glucose in the blood that cannot be properly absorbed by the body. The excess glucose spills into the urine, drawing water with it and increasing the volume of urine. This can lead to dehydration and electrolyte imbalances if left untreated.

In kidney disease, polyuria can be caused by damage to the kidneys that impairs their ability to concentrate urine. As a result, the body produces more urine than usual to compensate for the lack of concentrating ability.

Polyuria can also be a symptom of certain endocrine disorders such as diabetes insipidus, where the body produces too much antidiuretic hormone (ADH) or vasopressin, which leads to an excessive amount of urine production.

To diagnose polyuria, a healthcare provider may perform a physical examination, take a medical history, and conduct diagnostic tests such as urinalysis, blood glucose testing, and imaging studies. Treatment for polyuria depends on the underlying cause and may include medication, lifestyle changes, and in some cases, dialysis.

Anatomy18

Organisms4

Diseases49

Chemicals and Drugs85

Analytical, Diagnostic and Therapeutic Techniques and Equipment63

Phenomena and Processes39

Disciplines and Occupations1

Technology, Industry, Agriculture1

Information Science3

Named Groups4

Health Care30

Geographicals3

Acute renal failure caused by nephrotoxins. (1/6121)

Renal function tests: what do they mean? A review of renal anatomy, biochemistry, and physiology. (2/6121)

NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. (3/6121)

Recovery following relief of unilateral ureteral obstruction in the neonatal rat. (4/6121)

Plasma total homocysteine and cysteine in relation to glomerular filtration rate in diabetes mellitus. (5/6121)

Acute haemodynamic and proteinuric effects of prednisolone in patients with a nephrotic syndrome. (6/6121)

Antiproteinuric efficacy of verapamil in comparison to trandolapril in non-diabetic renal disease. (7/6121)

Hyperhomocyst(e)inaemia in children with chronic renal failure. (8/6121)

Glomerular Filtration Rate

Kidney

Creatinine

Kidney Function Tests

Kidney Diseases

Cystatin C

Inulin

Renal Circulation

Renal Insufficiency, Chronic

Technetium Tc 99m Pentetate

Iothalamic Acid

Albuminuria

Kidney Failure, Chronic

Natriuresis

Proteinuria

Renal Insufficiency

Diuresis

Kidney Glomerulus

Kidney Tubules

Blood Pressure

Renal Plasma Flow

Diabetic Nephropathies

Cystatins

Nephrons

Filtration

Iohexol

Radioisotope Renography

Sodium

Biological Markers

Chromium Radioisotopes

Nephrectomy

Kidney Transplantation

Acute Kidney Injury

Glomerular Filtration Barrier

Chronic Disease

Risk Factors

Hypertension

Hemodynamics

Follow-Up Studies

Metabolic Clearance Rate

p-Aminohippuric Acid

Renal Artery Obstruction

Aminohippuric Acids

Time Factors

Furosemide

Renin

Prospective Studies

Renal Plasma Flow, Effective

Retrospective Studies

Kidney Tubules, Proximal

Hypertension, Renal

Dogs

Cohort Studies

Cross-Sectional Studies

Renal Artery

Urine

Disease Progression

Punctures

Predictive Value of Tests

Angiotensin-Converting Enzyme Inhibitors

Water-Electrolyte Balance

Absorption

Nephrosclerosis

Uric Acid

Electrolytes

Vascular Resistance

Kidney Cortex

Diuretics

Kidney Concentrating Ability

Prognosis

Antihypertensive Agents

Plasma Volume

Hypertension, Renovascular

Atrial Natriuretic Factor

Diabetes Mellitus, Type 2

Pentetic Acid

Body Surface Area

Treatment Outcome

Edetic Acid

Captopril