Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors. Three PPAR isoforms, designated PPAR-alpha, beta/delta and -gamma, have been identified and were initially investigated in the tissues along urinary tract because of their known role in regulating lipid-activated gene transcription, lipid metabolism, inflammation and cell proliferation and differentiation. Gene distribution studies suggested that 3 PPAR isoforms are differentially expressed in the kidney. PPAR-alpha is predominantly expressed in renal proximal tubules and medullary thick ascending limbs. PPAR-gamma is mainly localized in renal medullary collecting duct with lower expression in renal glomeruli and renal microvasculature. Unlike PPAR-alpha and -gamma, PPAR-beta/delta is ubiquitously expressed in every segment along the nephron. In ureter and urinary bladder, all PPAR isoforms are mainly localized in urothelium of ureter and bladder. The emerging data have suggested physiological and pathophysiological roles of PPARs in tissues along urinary tract. PPAR-alpha plays a major role in triggering fatty acid utilization and the adaptive response to dietary lipids in the kidney. PPAR-beta/delta contributes to cell survival of renal interstitial cell in medullary hyperosmality. PPAR-gamma is involved in regulating renal hemodynamic and water and sodium transport. Furthermore, it also participates in the pathogenesis of glomerulopathy, antidiabetic thiazolidinedione-related water and sodium retention and renal, bladder and prostate carcinomas. PPARs may serve as potential therapeutic targets for certain diseases along urinary tract including glomerulosclerosis, diabetic nephropathy and kidney, prostate and bladder tumors.
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PMID:Targeting peroxisome proliferator-activated receptors (PPARs) in kidney and urologic disease. 1218 90

Nonsteroid antiinflammatory drugs have been implicated as nephrotoxic drugs, causing both acute and chronic adverse effects that range from reversible ischemia to chronic kidney disease and urothelial tumors to renal cell carcinoma specially papillary subtype. We report one case of collecting duct (Bellini duct) renal cell carcinoma in patient with analgesic-abuse nephropathy. This young individual was suffering from ankylosing spondylitis since the age of 16 years and was consuming diclofenac and paracetamol (acetaminophen) combination for >15 years. He developed hypertension, secondary glomerulopathy, chronic kidney disease and collecting duct renal cell carcinoma.
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PMID:Can Analgesic-abuse Nephropathy is a Fertile Groundfor for Rare Collecting Duct (Bellini Duct) Renal Cell Carcinoma or Merely a Coincidence? 2716 95

Idiopathic nephrotic syndrome is the most common glomerulopathy in childhood characterised by heavy proteinuria, hypoalbuminemia and edema. Most of the patients have mild and transient edema but those with difficult to treat nephrotic syndrome can develop severe edema which may have serious consequences such as immobility, cellulitis and peritonitis. Understanding of the pathophysiology of edema is still evolving with recent research elucidating newer mechanism of sodium retention through plasmin mediated epithelial sodium channel activation in collecting duct. Patients with mild edema do not require specific diuretic therapy as it improves with steroid induced diuresis. In this review, the authors describe the current perspective in management of moderate to severe edema in childhood nephrotic syndrome including various parameters to assess intravascular volume status which is important for planning overall treatment strategy. Then they briefly discuss about various classes of diuretics, aquaretics and evidence based use of furosemide albumin combination therapy for treatment of edema. Management strategy for a small proportion of patients, who are unresponsive to furosemide therapy, includes diuretic synergism, intravenous furosemide albumin combination therapy and continuous intravenous furosemide infusion.
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PMID:Current Perspectives in Management of Edema in Nephrotic Syndrome. 3223 33