Kidney Tubules, Proximal
Kidney Tubules, Collecting
Kidney Tubules, Distal
Acute Kidney Injury
Molecular Sequence Data
Kidney Failure, Chronic
Polycystic Kidney Diseases
Kidney Function Tests
Polycystic Kidney, Autosomal Dominant
Kidney Concentrating Ability
Acute renal failure caused by nephrotoxins. (1/3275)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)
Methoxyflurane nephropathy. (2/3275)Investigations of methoxyflurane-induced nephrotoxicity in man have been extensively aided by the use of an animal model. To be of value the animal model must share similar metabolic pathways with man and have the same clinical manifestations of the diseases process. The Fischer 344 rat appears to meet these criteria. The predominant factors in the production of methoxyflurane nephrotoxicity appear to be high methoxyflurane dosage and serum inorganic fluoride concentration. It is likely that secondary factors include: (1) a high rate of methoxyflurane metabolism and sepsitivity of the kidney to inorganic fluoride toxicity: (2) concurrent treatment with other nephrotoxic drugs; (3) preexisting renal disease; (4) surgery of the urogenital tract, aorta, or renal vasculative; (5) repeat administration of methoxyflurane due to accumulation of inorganic fluoride and, perhaps, methoxyflurane induction of its own metabolism: and (6) concurrent treatment with enzyme-inducing drugs such as phenobarbital. (+info)
Renal function tests: what do they mean? A review of renal anatomy, biochemistry, and physiology. (3/3275)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)
The surface ectoderm is essential for nephric duct formation in intermediate mesoderm. (4/3275)The nephric duct is the first epithelial tubule to differentiate from intermediate mesoderm that is essential for all further urogenital development. In this study we identify the domain of intermediate mesoderm that gives rise to the nephric duct and demonstrate that the surface ectoderm is required for its differentiation. Removal of the surface ectoderm resulted in decreased levels of Sim-1 and Pax-2 mRNA expression in mesenchymal nephric duct progenitors, and caused inhibition of nephric duct formation and subsequent kidney development. The surface ectoderm expresses BMP-4 and we show that it is required for the maintenance of high-level BMP-4 expression in lateral plate mesoderm. Addition of a BMP-4-coated bead to embryos lacking the surface ectoderm restored normal levels of Sim-1 and Pax-2 mRNA expression in nephric duct progenitors, nephric duct formation and the initiation of nephrogenesis. Thus, BMP-4 signaling can substitute for the surface ectoderm in supporting nephric duct morphogenesis. Collectively, these data suggest that inductive interactions between the surface ectoderm, lateral mesoderm and intermediate mesoderm are essential for nephric duct formation and the initiation of urogenital development. (+info)
Decreased expression of the pro-apoptotic protein Par-4 in renal cell carcinoma. (5/3275)Par-4 is a widely expressed leucine zipper protein that confers sensitization to apoptosis induced by exogenous insults. Because the expression of genes that promote apoptosis may be down-regulated during tumorigenesis, we sought to examine the expression of Par-4 in human tumors. We present here evidence that Par-4 protein levels were severely decreased in human renal cell carcinoma specimens relative to normal tubular cells. Replenishment of Par-4 protein levels in renal cell carcinoma cell lines conferred sensitivity to apoptosis. Because apoptosis may serve as a defense mechanism against malignant transformation or progression, decreased expression of Par-4 may contribute to the pathophysiology of renal cell carcinoma. (+info)
T lymphocyte adhesion mechanisms within inflamed human kidney: studies with a Stamper-Woodruff assay. (6/3275)Renal inflammatory conditions are characterized by mononuclear cell recruitment to sites of inflammation. We have developed a modified Stamper-Woodruff assay system to analyze mechanisms of functional T cell adhesion to cryostat sections of renal biopsy material from patients with vasculitic glomerulonephritis (GN) and acute allograft rejection. Peripheral blood T cells adhered to intraglomerular, periglomerular, and tubulointerstitial regions of the cortex. Blocking monoclonal antibodies against tissue expressed ICAM-1, VCAM-1, and the CS-1 domain of fibronectin (CS-1Fn) differentially attenuated T cell adhesion. Glomerular adhesion in vasculitic GN and tubulointerstitial adhesion in acute rejection were particularly sensitive to both anti-ICAM-1 and anti-VCAM-1 antibodies, indicating a prominent role for ICAM-1 and VCAM-1 at glomerular sites in vasculitis and at tubulointerstitial sites in rejection. Furthermore, using KL/4 cells (LFA-1 expressing) and Jurkat cells (VLA-4 expressing), we demonstrated specific LFA-1/ICAM-1- and VLA-4/VCAM-1-mediated interactions within glomerular and tubulointerstitial compartments. Jurkat cells also adhered to VCAM-1-free sites, and binding was inhibitable by anti-CS-1Fn antibody, thereby demonstrating a role for VLA-4/fibronectin interactions especially at intraglomerular sites in acute rejection where VCAM-1 is notably absent. We therefore propose a prominent functional role for ICAM-1, VCAM-1, and CS-1 domain fibronectin in T cell recruitment to the inflamed kidney. (+info)
Recovery following relief of unilateral ureteral obstruction in the neonatal rat. (7/3275)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)
Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy. (8/3275)BACKGROUND: Proteinuria and tubular atrophy have both been closely linked with progressive renal failure. We hypothesized that apoptosis may be induced by tubular cell exposure to heavy proteinuria, potentially leading to tubular atrophy. Apoptosis was studied in a rat model of "pure" proteinuria, which does not induce renal impairment, namely protein-overload proteinuria. METHODS: Adult female Lewis rats underwent intraperitoneal injection of 2 g of bovine serum albumin (BSA, N = 16) or sham saline injections (controls, N = 8) daily for seven days. Apoptosis was assessed at day 7 in tissue sections using in situ end labeling (ISEL) and electron microscopy. ISEL-positive nuclei (apoptotic particles) were counted in blinded fashion using image analysis with NIH Image. Cell proliferation was assessed by detection of mRNA for histone by in situ hybridization, followed by counting of positive cells using NIH Image. RESULTS: Animals injected with saline showed very low levels of apoptosis on image analysis. BSA-injected rats had heavy proteinuria and showed both cortical and medullary apoptosis on ISEL. This was predominantly seen in the tubules and, to a lesser extent, in the interstitial compartment. Overall, the animals injected with BSA showed a significant 30-fold increase in the number of cortical apoptotic particles. Electron microscopy of tubular cells in a BSA-injected animal showed a progression of ultrastructural changes consistent with tubular cell apoptosis. The BSA-injected animals also displayed a significant increase in proximal tubular cell proliferation. This increased proliferation was less marked than the degree of apoptosis. CONCLUSION: Protein-overload proteinuria in rats induces tubular cell apoptosis. This effect is only partially balanced by proliferation and potentially provides a direct mechanism whereby heavy proteinuria can induce tubular atrophy and progressive renal failure. (+info)
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 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.
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).
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.
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.
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.
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 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.
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.
There are two main types of PKD: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). ADPKD is the most common form of PKD and accounts for about 90% of all cases. It is caused by mutations in the PKD1 or PKD2 genes, which are inherited from one's parents. ARPKD is less common and is caused by mutations in the PKHD1 gene.
The symptoms of PKD can vary depending on the severity of the disease and the age of onset. Common symptoms include high blood pressure, back pain, kidney stones, urinary tract infections, and frequent urination. As the cysts grow, they can also cause complications such as kidney damage, anemia, and electrolyte imbalances.
PKD is typically diagnosed through a combination of imaging tests such as ultrasound, CT scans, and MRI, as well as genetic testing to identify the presence of the disease-causing mutations. There is no cure for PKD, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control high blood pressure, pain management, and dialysis in advanced cases.
In conclusion, polycystic kidney disease (PKD) is a genetic disorder that affects the kidneys and can lead to chronic kidney disease and eventually kidney failure. It is important to be aware of the symptoms and risk factors for PKD, as well as to seek medical attention if they are present, in order to receive proper diagnosis and treatment.
Symptoms of Kidney Neoplasms can include blood in the urine, pain in the flank or abdomen, weight loss, fever, and fatigue. Diagnosis is made through a combination of physical examination, imaging studies such as CT scans or ultrasound, and tissue biopsy. Treatment options vary depending on the type and stage of the neoplasm, but may include surgery, ablation therapy, targeted therapy, or chemotherapy.
It is important for individuals with a history of Kidney Neoplasms to follow up with their healthcare provider regularly for monitoring and check-ups to ensure early detection of any recurrences or new tumors.
There are several types of kidney calculi, including:
1. Calcium oxalate calculi: These are the most common type of calculus and are often associated with conditions such as hyperparathyroidism or excessive intake of calcium supplements.
2. Uric acid calculi: These are more common in people with gout or a diet high in meat and sugar.
3. Cystine calculi: These are rare and usually associated with a genetic disorder called cystinuria.
4. Struvite calculi: These are often seen in women with urinary tract infections (UTIs).
Symptoms of kidney calculi may include:
1. Flank pain (pain in the side or back)
2. Pain while urinating
3. Blood in the urine
4. Cloudy or strong-smelling urine
5. Fever and chills
6. Nausea and vomiting
Kidney calculi are diagnosed through a combination of physical examination, medical history, and diagnostic tests such as X-rays, CT scans, or ultrasound. Treatment options for kidney calculi depend on the size and location of the calculus, as well as the severity of any underlying conditions. Small calculi may be treated with conservative measures such as fluid intake and medication to help flush out the crystals, while larger calculi may require surgical intervention to remove them.
Preventive measures for kidney calculi include staying hydrated to help flush out excess minerals in the urine, maintaining a balanced diet low in oxalate and animal protein, and avoiding certain medications that can increase the risk of calculus formation. Early detection and treatment of underlying conditions such as hyperparathyroidism or gout can also help prevent the development of kidney calculi.
Overall, kidney calculi are a common condition that can be managed with proper diagnosis and treatment. However, they can cause significant discomfort and potentially lead to complications if left untreated, so it is important to seek medical attention if symptoms persist or worsen over time.
DNA-binding protein from starved cells
Induced stem cells
Hypertensive kidney disease
Monovalent cation:proton antiporter-1
Friedrich Gustav Jakob Henle
GABA transporter type 2
Acute tubular necrosis
Diffuse proliferative nephritis
Fibroblast growth factor 23
Pharmacology of bicalutamide
Albright's hereditary osteodystrophy
Autosomal dominant polycystic kidney disease
RAT AND CANINE MICROPHYSIOLOGICAL SYSTEMS OF THE KIDNEY PROXIMAL TUBULE FOR CHEMICAL TOXICITY SCREENING
The Hydrogen-Coupled Oligopeptide Membrane Cotransporter Pept2 is SUMOylated in Kidney Distal Convoluted Tubule Cells - PubMed
Kidney Tubules Expression Atlas
Publication: Effect of Intensive Blood Pressure Lowering on Kidney Tubule Injury: …
Associations of Urine Biomarkers of Kidney Tubule Health With Incident Hypertension and Longitudinal Blood Pressure Change in...
Endothelin-1 increases rat distal tubule acidification in vivo
RTECS:WB0350000 - Sodium fluoride - The Registry of Toxic Effects of Chemical Substances | CDC/NIOSH
New 3-D model offers insights into the role of glucose in a deadly kidney disease | National Institutes of Health (NIH)
Help Save & pel the structures seen in the photomicrograph of the kidney. Glomerular capsule Glomerulus Renal tubule Renal |...
downloadable PDF v
American Society of Nephrology | Kidney Week - Abstract Details (2018)
Acute kidney failure: MedlinePlus Medical Encyclopedia
Susanne E. Churchill, Ph.D. | Harvard Catalyst Profiles | Harvard Catalyst
RTECS:JM5690000 - Dipyrido(1,2-a;2',1'-c)pyrazinediium, 6,7-dihydro-, dibromide - The Registry of Toxic Effects of Chemical...
Advanced Search Results - Public Health Image Library(PHIL)
Proteinuria: Practice Essentials, Pathophysiology, Etiology
Renal Cortical Necrosis: Background, Etiology, Epidemiology
Recombinant Anti-Integrin alpha V antibody [EPR16800] (ab179475) | Abcam
RFA-RM-11-022: Integrated Microphysiological Systems for Drug Efficacy and Toxicity Testing in Human Health and Disease (UH2...
Liver Failure (Acute) in Cats | PetMD
Medullary Sponge Kidney - NIDDK
JCI Insight - Hnf4a deletion in the mouse kidney phenocopies Fanconi renotubular syndrome
JCI - Kidney injury molecule-1 is a phosphatidylserine receptor that confers a phagocytic phenotype on epithelial cells
Frontiers | Differentiated mouse kidney tubuloids as a novel in vitro model to study collecting duct physiology
- Figure Legend: Figure 1 Kidney, Renal tubule - Regeneration in a male rat from an acute study. (nih.gov)
- Renal tubule regeneration occurs as a reparative response to previous degeneration and/or necrosis of renal tubular epithelium. (nih.gov)
- This database provides expression level of proteins in each renal tubule segment. (nih.gov)
- Each renal tubule segment was microdissected from male Sprague Dawley rats and analysed with Orbitrap Lumos mass spectrometry. (nih.gov)
- Transcriptome data of microdissected renal tubule from Lee et al. (nih.gov)
- Quantitative Proteomics of All 14 Renal Tubule Segments in Rat. (nih.gov)
- Figure Legend: Figure 1 Kidney, Renal tubule - Dilation in a male B6C3F1 mouse from a chronic study. (nih.gov)
- Kidney, Renal tubule - Dilation in a male F344/N rat from a chronic study. (nih.gov)
- Renal tubule dilation may occur anywhere along the nephron or collecting duct system. (nih.gov)
- Renal tubule dilation may occur from xenobiotic administration, secondary mechanisms, or an unknown pathogenesis (see Kidney - Nephropathy, Obstructive (Figure 2). (nih.gov)
- Renal tubule dilation should be diagnosed and given a severity grade. (nih.gov)
- 1. Renal tubule. (nursingpaperhub.com)
- Overflow proteinuria is most commonly associated with increased production of abnormal low molecular weight proteins (eg, light chains in multiple myeloma, myoglobin in rhabdomyolysis) that exceeds the reabsorption capacity of the proximal tubule, leading to spilling of the protein into the urine. (medscape.com)
- Dysfunction of the proximal tubule segment can lead to Fanconi renotubular syndrome (FRTS), with major symptoms such as excess excretion of water, glucose, and phosphate in the urine. (jci.org)
- Furthermore, we show that loss of Hnf4a decreased the expression of proximal tubule-specific genes. (jci.org)
- Analysis of the adult Hnf4a mutant kidney also showed proximal tubule dysgenesis and nephrocalcinosis. (jci.org)
- Our results demonstrate the critical role of Hnf4a in proximal tubule development and provide mechanistic insight into the etiology of FRTS. (jci.org)
- Kidneys are composed of multiple nephron segments: the proximal tubule (PT), the loop of Henle (LoH), distal convoluted tubule (DCT), connecting tubule (CNT) and finally the most distal part of the nephron, the collecting duct (CD) ( Alpern and Hebert, 2007 ). (frontiersin.org)
- Different nephron tubule segments perform distinct physiological functions, collectively acting as a blood filtration unit. (jci.org)
- One of our major goals is to target the mechanisms by which the Wnt signal transduction triggers the developmental program that leads to formation of the functional of the kidney, the nephron. (oulu.fi)
- At present we can study in detail the major considered cell types that assemble the kidney, namely epithelial ureteric bud, nephron progenitors, stromal cells and endothelial cells. (oulu.fi)
- Using mass spectrometry-based proteomics, 1037 SUMO1 and 552 SUMO2 sites, corresponding to 546 SUMO1 and 356 SUMO2 proteins, were identified from a modified mouse kidney DCT cell line (mpkDCT). (nih.gov)
- Using immunolabelling of mouse kidney sections Pept2 was localized to DCT cells in vivo . (nih.gov)
- IHC: Human kidney, human transitional cell carcinoma of bladder and mouse kidney tissues. (abcam.com)
- Here, we found that Hnf4a is expressed in both presumptive and differentiated proximal tubules in the developing mouse kidney. (jci.org)
- This illustrates the potential use of mouse kidney tubuloids as novel in vitro models to study (patho)physiology of kidney diseases. (frontiersin.org)
- drug-induced nephrotoxicity is a major health concern that contributes to 25% of all cases of severe acute kidney failure. (nih.gov)
- Acute kidney failure is the rapid (less than 2 days) loss of your kidneys' ability to remove waste and help balance fluids and electrolytes in your body. (medlineplus.gov)
- Contact your provider if your urine output slows or stops or you have other symptoms of acute kidney failure. (medlineplus.gov)
- For patient education information, see Acute Kidney Failure . (medscape.com)
- Damage to the kidneys may cause signs of acute kidney failure such as increased thirst, increased urination, vomiting, diarrhea, loss of appetite, lethargy and dilute urine (lighter in color). (petplace.com)
- Additionally, this test measures kidney values such as the creatinine and blood urea nitrogen (BUN), which are elevated if acute kidney failure is present. (petplace.com)
- Animals with acute kidney failure typically exhibit dilute urine due to the inability of the kidneys to concentrate the urine. (petplace.com)
- While much is known about the genetic causes of PKD, Freedman and team realized there's much still much to learn about the basics of how cysts form in the kidney's tiny tubes, or tubules , that help to filter toxins out of the bloodstream. (nih.gov)
- The kidney gets bigger, and as the tubules widen to accommodate the expansion over time, cysts form," Freedman said. (nih.gov)
- In medullary sponge kidney, tiny, fluid-filled sacs called cysts form in the tubules within the medulla-the inner part of the kidney-creating a spongelike appearance. (nih.gov)
- Scientists do not fully understand the cause of medullary sponge kidney or why cysts form in the tubules during fetal development. (nih.gov)
- An individual with proteinuria in the setting of a normal glomerular filtration rate (GFR) is at high risk of progressive loss of kidney function. (medscape.com)
- The reduction in the glomerular filtration rate (GFR) that occurs from ischemic injury is a result not only of reduced filtration due to hypoperfusion but also of casts and debris obstructing the tubule lumen, causing back-leak of filtrate through the damaged epithelium (ie, ineffective filtration). (medscape.com)
- Whereas allopurinol is cleared essentially by glomerular filtration, oxipurinol is reabsorbed in the kidney tubules in a manner similar to the reabsorption of uric acid. (nih.gov)
- Because endothelin receptor inhibition blunts increased distal tubule acidification induced by dietary acid, we examined whether endothelin-1 (ET-1) increases acidification of in vivo perfused distal tubules of anesthetized rats. (nih.gov)
- Angiotensin II stimulated Epo mRNA expression in proximal and distal tubules but not in the interstitial cells. (asn-online.org)
- Kidney injury molecule-1 (KIM-1 or TIM-1) is an immunoglobulin superfamily cell-surface protein not expressed by cells of the myeloid lineage but highly upregulated on the surface of injured kidney epithelial cells. (jci.org)
- Here we demonstrate that injured kidney epithelial cells assumed attributes of endogenous phagocytes. (jci.org)
- Kidney tubuloids are cell models that are derived from human or mouse renal epithelial cells and show high similarities with their in vivo counterparts. (frontiersin.org)
- It is found in membranes of intestinal epithelial cells, proximal kidney tubules and liver hepatocytes. (collie-online.com)
- Regeneration following acute tubule epithelial injury is characterized by flattened epithelium and tubule epithelial cell basophilia and is accompanied by nuclear crowding. (nih.gov)
- Dilation may result from direct toxic injury to the tubule epithelium interfering with absorption and secretion (Figure 3). (nih.gov)
- Slight tubule dilation is associated with degeneration and necrosis. (nih.gov)
- Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in the renal category (that is, AKI in which the pathology lies within the kidney itself). (medscape.com)
- The term ATN is actually a misnomer, as there is minimal cell necrosis and the damage is not limited to tubules. (medscape.com)
- Similar mechanisms are involved in the reabsorption of these nutrients after they have been filtered from the blood by the kidneys. (oregonstate.edu)
- EXPOSURES: Urine biomarkers of tubular injury (kidney injury molecule 1, interleukin 18 [IL-18]), repair (human cartilage glycoprotein 39 [YKL-40]), and inflammation (monocyte chemoattractant protein 1) at baseline and year 2. (nih.gov)
- Associations of Urine Biomarkers of Kidney Tubule Health With Incident Hypertension and Longitudinal Blood Pressure Change in Middle-Aged Adults: The CARDIA Study. (bvsalud.org)
- Urine biomarkers of kidney tubule injury associate with incident hypertension in older adults with comorbidities, but less is known about these associations in younger adults . (bvsalud.org)
- A team led by Johns Hopkins Medicine researchers says it has identified two protein biomarkers in urine that may one day be used to better diagnose acute interstitial nephritis (AIN), an underdiagnosed but treatable kidney disorder that impairs renal function in the short term and can lead to chronic kidney disease, permanent damage or renal failure if left unchecked. (hopkinsmedicine.org)
- He says the hope is that later, biomarkers can replace kidney biopsies altogether. (hopkinsmedicine.org)
- These patients require close follow-up and may need a kidney biopsy if they have abnormal urine microscopy results and/or impairment of kidney function. (medscape.com)
- Photomicrograph of a kidney biopsy specimen shows renal medulla, which is composed mainly of renal tubules. (medscape.com)
- Knowing that cytokines - proteins secreted by immune cells known as CD4+ T lymphocytes - are the agents causing inflammation of the tubules, the researchers measured the amounts of 12 urine and 10 blood plasma proteins in samples from 79 adult, biopsy-confirmed AIN patients, and compared them to the amounts in 186 adult kidney biopsy patients without an AIN diagnosis. (hopkinsmedicine.org)
- An ultrasound-guided biopsy of the liver or kidneys may be necessary to determine the extent of damage to these organs or to confirm that Rimadyl® is the cause of the damage. (petplace.com)
- The histologic cross section of healthy kidney tissue on the left shows renal tubules (one seen within yellow circle) that reabsorb water and organic materials while secreting wastes. (hopkinsmedicine.org)
- Using this one-two approach at the lab bench, the researchers modeled in just a few weeks different aspects of the fluid-filled cysts that form in polycystic kidney disease (PKD ), a common cause of kidney failure. (nih.gov)
- Mini-kidney tube structures have sugar receptors (red, upper left) and form outward-facing polycystic kidney disease cysts (center image), which swell by taking in sugar (green, lower right). (nih.gov)
- A research team supported by the National Institutes of Health has developed a new approach to better understand the biology of polycystic kidney disease (PKD), an often-life-threatening genetic disorder that affects millions worldwide. (nih.gov)
- 2004. Osteogenic protein-1 (rhOP-1) treatment induces tubular regeneration in the acute and chronic phases of the rat remnant kidney model. (nih.gov)
- Tubule dilation is associated with chronic progressive nephropathy. (nih.gov)
- Secondary mechanisms of tubule dilation may result from lower urinary tract obstruction, the deposition of tubule crystals, interstitial inflammation and/or fibrosis, and chronic progressive nephropathy (Figure 4). (nih.gov)
- LIMITATIONS: Few participants with advanced baseline chronic kidney disease. (nih.gov)
- The 2012 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for the evaluation and management of chronic kidney disease (CKD) includes proteinuria in the staging of CKD. (medscape.com)
- 11. The STAT1/HMGB1/NF-κB pathway in chronic inflammation and kidney injury after cisplatin exposure. (nih.gov)
- Medullary sponge kidney rarely leads to more serious problems, such as chronic kidney disease or kidney failure . (nih.gov)
- You will be told what you may and may not eat to reduce the buildup of toxins that the kidneys would normally remove. (medlineplus.gov)
- In middle-aged adults without hypertension , cardiovascular disease , or kidney disease , higher urine EGF associated with lower risk of incident hypertension and lower 10-year BP elevations. (bvsalud.org)
- The detection of proteins excreted in the urine has been extensively used in the assessment of kidney diseases. (medscape.com)
- Transient proteinuria occurs in persons with normal kidney function, bland urine sediment, and normal blood pressure. (medscape.com)
- In a normal kidney , urine flows through these tubules as the kidney is being formed during a fetus' growth. (nih.gov)
- The cysts keep urine from flowing freely through the tubules. (nih.gov)
- No physical signs are usually present in a patient with medullary sponge kidney, except for blood in the urine. (nih.gov)
- The kidneys excrete the contrast medium into urine, which makes the urine visible on an x-ray. (nih.gov)
- As a result, the tubules cannot properly reabsorb water and useful organic substances, such as glucose and amino acids, or secrete waste products such as urea and creatinine into urine. (hopkinsmedicine.org)
- The urine is also evaluated for the presence of casts, which, if present, indicate that a region of the kidneys called the tubules has been damaged. (petplace.com)
- This ADH assists the kidneys control the quantity of water the body loses through the urine. (differencebetween.net)
- In this study, we investigated the localization of Epo protein-producing cells in the kidney and liver after fludrocortisone injection. (asn-online.org)
- Western blot showed that Epo protein expression was increased by 5-fold in the kidney but not changed in the liver. (asn-online.org)
- Rimadyl® toxicity can cause damage to the gastrointestinal tract, liver and kidneys. (petplace.com)
- Idiosyncratic reactions usually cause damage to the liver specifically but can also affect the kidneys and gastrointestinal tract. (petplace.com)
- An abdominal ultrasound is performed to evaluate the kidneys and the liver. (petplace.com)
- To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world. (asn-online.org)
- A few dilated tubules may be regarded as normal histologic variation. (nih.gov)
- On the right, a cross section of a kidney impacted by acute interstitial nephritis shows inflammation and swelling of the tubules (as seen within the black circle). (hopkinsmedicine.org)
- Acute interstitial nephritis is a condition marked by inflammation and swelling of the renal tubules, the tiny portals in the kidneys where blood is filtered. (hopkinsmedicine.org)
- 3. Signaling Rho-kinase mediates inflammation and apoptosis in T cells and renal tubules in cisplatin nephrotoxicity. (nih.gov)
- 7. Dexmedetomidine protects against cisplatin-induced acute kidney injury in mice through regulating apoptosis and inflammation. (nih.gov)
- 18. Asiatic acid protects against cisplatin-induced acute kidney injury via anti-apoptosis and anti-inflammation. (nih.gov)
- To find such a biomarker, Parikh and his colleagues looked for a substance linked to AIN's most distinct characteristic, inflammation of the renal tubules, formally known as tubulitis. (hopkinsmedicine.org)
- A kidney or abdominal ultrasound is the preferred test for diagnosing a blockage in the urinary tract. (medlineplus.gov)
- ET-1 was infused intraaortically (1.4 pmol x kg(-1) x min[-1]) into control animals and into those with increased distal tubule HCO3 secretion induced by drinking 80 mM NaHCO3 solution for 7-10 days. (nih.gov)
- The data show that ET-1 increases distal tubule acidification in vivo and can do so by increasing H+ secretion and by decreasing HCO3 secretion when the latter is augmented by dietary NaHCO3. (nih.gov)
- In Diabetes insipidus (DI), there is either lowered production of Antidiuretic hormone (central DI), or normal Antidiuretic hormone secretion with resistance in the kidneys to its impacts (nephrogenic Diabetes insipidus). (differencebetween.net)
- To understand cyst formation better, Freedman's team and others have invented methods to grow human kidney organoids, complete with a system of internal tubules. (nih.gov)
- Combining PKD organoids with kidney-on-a-chip technology provided the best of both worlds. (nih.gov)
- The researchers think that the tubules are taking in fluid in the mice just as they do in the organoids. (nih.gov)
- We think the tubules are taking in fluid in the mice, just like in the organoids. (nih.gov)
- Help Save & pel the structures seen in the photomicrograph of the kidney. (nursingpaperhub.com)
Types of kidney disease2
- Hyponatremia (abnormally low sodium concentrations in blood) is common among older adults and in individuals with hypertension , kidney disease, and heart disease. (oregonstate.edu)
- We're able to boil down a complex process of cyst formation in tubules into a process in a petri dish that takes just a few weeks, but there's been a lack of technologies to study the disease further," said University of Washington School of Medicine scientist Benjamin Freedman, Ph.D., who led the work. (nih.gov)
- Proteinuria identifies patients with kidney damage and those at risk for worsening kidney disease and increased cardiovascular morbidity. (medscape.com)
- Tubular proteinuria is a result of tubulointersitial disease affecting the proximal renal tubules and interstitium. (medscape.com)
- In addition, STAT3 activation due to lysosomal stress likely explains the hyperproliferative kidney disease and splenomegaly observed in AEP-deficient mice. (nature.com)
- The disease is estimated to cause 15 to 20% of all hospitalizations for acute kidney injury. (hopkinsmedicine.org)
- Although glucose is generally absorbed by the kidneys, glucose absorption has not been connected to cyst formation in PKD. (nih.gov)
- It may occur in focal areas or as tracts running along the entire length of kidney sections (Figure 1). (nih.gov)
- Various mechanisms act on the kidney to ensure that the amount of sodium lost via renal excretion compensates adequately for the amount of sodium consumed, thereby maintaining sodium homeostasis . (oregonstate.edu)
- Additional adverse health outcomes, including gastric cancer , osteoporosis , and kidney stones , have also been linked to sodium overconsumption. (oregonstate.edu)
- Each human kidney has millions of tubules, and in people with PKD, some of them expand gradually and abnormally to form sacs of fluid that researchers liken to water balloons. (nih.gov)
- The researchers have shown that simulating fluid flow is essential to making this system more like the environment in the kidney with PKD," said Danilo Tagle, Ph.D., director of the NCATS Office of Special Initiatives. (nih.gov)
- Researchers have reported that 12 to 20 percent of people who develop calcium-based kidney stones have medullary sponge kidney. (nih.gov)
- The tubule cell damage and cell death that characterize ATN usually result from an acute ischemic or toxic event. (medscape.com)
- These sacs, or cysts, crowd out healthy tissue, leading over time to reduced kidney function and, in some instances, complete kidney failure. (nih.gov)
- The PKD cysts arise and grow as the kidney tissue works to retain most of the fluids that constantly pass through them. (nih.gov)
- The sacs, or cysts, eventually crowd out healthy tissue, leading to problems in kidney function and kidney failure. (nih.gov)
- 5. Sphingosine kinase 2 cooperating with Fyn promotes kidney fibroblast activation and fibrosis via STAT3 and AKT. (nih.gov)
- At any given moment, about a quarter of all the fluids in the body pass through the kidneys, and this constant flow was missing from the organoid. (nih.gov)
- They also contain a network of microfluidic channels to replicate the natural flow of fluids in a living kidney. (nih.gov)
- However, the cysts don't develop from fluids that the kidneys outwardly secrete, as long thought. (nih.gov)
- The kidneys maintain homeostasis of fluids and electrolytes, remove waste products from the blood and regulate blood acid-base balance ( Alpern and Hebert, 2007 ). (frontiersin.org)
- Intravenous fluids are administered at high rates (diuresis) to rehydrate pets that are dehydrated from vomiting and diarrhea and to treat or prevent kidney failure. (petplace.com)
- Injury of tubular cells is most prominent in the straight portion of the proximal tubules and in the thick ascending limb of the loop of Henle, especially as it dips into the relatively hypoxic medulla. (medscape.com)
- 10. NF-κB transcriptional inhibition ameliorates cisplatin-induced acute kidney injury (AKI). (nih.gov)
- Anticancer drug-induced kidney disorders. (nih.gov)
- We have during the past few years developed novel ex vivo technologies to get better access to study the cellular and molecular basic of kidney organogenesis. (oulu.fi)
- In addition to the in vivo approaches we have gained skills to dissociate the embryonic kidney mesenchyme to single cells and yet to regenerate the potential for nephrogenesis and even the complete kidney organogenesis. (oulu.fi)
- Although scientists had known that kidneys absorb glucose, they'd never connected this process to the formation of cysts in PKD. (nih.gov)
- In further studies, the scientists gave fluorescently labeled glucose to mice with PKD and could see that kidney cysts in the animals also took up glucose. (nih.gov)
- 17. NLRP3 inflammasome knockout mice are protected against ischemic but not cisplatin-induced acute kidney injury. (nih.gov)
- These more complex 3D models, containing living kidney cells, aim to mimic more fully the kidney and its environment. (nih.gov)
- Additionally, we knew that IL-9 leads to the accumulation of mast cells that release histamine and other chemicals that induce allergic responses, and kidney biopsies from AIN patients frequently reveal the presence of mast cells," he adds. (hopkinsmedicine.org)
- Following an acute phase of tubule injury, regeneration is characterized by tubule basophilia, nuclear crowding, and increased mitoses. (nih.gov)
- Effect of Intensive Blood Pressure Lowering on Kidney Tubule Injury: Findings From the ACCORD Trial Study Participants. (nih.gov)
- Avoid drugs and medicines that can cause kidney injury. (medlineplus.gov)
- Weisbord SD, Palevsky PM. Prevention and management of acute kidney injury. (medlineplus.gov)
- 1. Loss of sphingosine kinase 2 protects against cisplatin-induced kidney injury. (nih.gov)
- 12. Blockade of histone deacetylase 6 protects against cisplatin-induced acute kidney injury. (nih.gov)
- 16. Autophagy in proximal tubules protects against acute kidney injury. (nih.gov)
- 19. Omeprazole attenuates cisplatin-induced kidney injury through suppression of the TLR4/NF-κB/NLRP3 signaling pathway. (nih.gov)
- Membrane proteomics, immunoblotting, high-resolution microscopy, and immunogold electron microscopy were used to analyze human and murine podocyte ADAM10 expression in health and kidney injury. (lww.com)
- While we are studying EVs in kidney organogenesis and skin and sensing, we also characterize EVs in other health conditions, such as cancers and brain function, and also in the nature via analysis of EVs in milk, berries, trees, and air filtrates. (oulu.fi)
- Other blood tests may be done to find the underlying cause of kidney failure. (medlineplus.gov)
- As cyst absorbs glucose passing through the tubule, it grows larger. (nih.gov)
- The pathologist should use his or her judgment in deciding whether or not secondary tubule dilation is prominent enough to warrant a separate diagnosis. (nih.gov)