Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrogenic diabetes insipidus (DI) secondary to chronic urinary tract obstruction is a rare disease. The exact cause is unknown but it is likely that increased collecting duct pressures cause damage to the tubular epithelium, resulting in insensitivity to the action of arginine-vasopressin (AVP). A 77-year-old man complaining of polyuria and polydipsia was treated with alpha glucosidase inhibitor under the impression of polyuria due to diabetes mellitus. But his symptoms did not improve. Water deprivation and AVP administration study revealed that the patient had nephrogenic DI. Urinary tract obstruction due to an enlarged prostate was suggested as a principal cause of nephrogenic DI. The patient underwent transurethral resection of the prostate and bilateral subcapsular orchiectomy. After surgery, the urine osmolarity was normalized and the patient became symptom-free. We report a case of nephrogenic DI due to obstructive uropathy which was cured by surgery eliminating obstruction.
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PMID:A case of nephrogenic diabetes insipidus caused by obstructive uropathy due to prostate cancer. 1073 36

Nephrogenic diabetes insipidus (NDI) results from the inability of the late distal tubules and collecting ducts to respond to vasopressin. The lack of ability to concentrate urine results in polyuria and polydipsia. Primary and acquired forms of NDI exist in children. Congenital NDI is a result of mutation in AVPR2 or AQP2 genes. Secondary NDI is associated with electrolyte abnormalities, obstructive uropathy, or certain medications. Management of NDI can be difficult with only symptomatic treatment available, using low-solute diet, diuretics, and prostaglandin inhibitors.
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PMID:Nephrogenic Diabetes Insipidus. 3045 45

Nephrogenic diabetes insipidus (NDI) is one of the principal defects leading to polyuria-polydipsia syndrome (PPS). In the absence of other evident causes (drug interaction, electrolytic disorders or inherited disease), obstructive uropathy is the most likely aetiology. Direct arginine vasopressin (AVP) assessment during water deprivation test (WDT) remains the gold standard in PPS differential diagnosis despite well characterised limitations in this procedure. A new WDT method using copeptin as reliable surrogate of AVP is proposed. This case represents the first report of an NDI due to idiopathic urethral stricture in an adult and it would like to be explicative of the importance of a correct differential diagnosis of PPS and of the risk related to a prolonged WDT procedure in a frail patient. A 48-year-old male patient presenting with polyuria and polydipsia lasting one month was diagnosed with NDI. Copeptin values were clearly elevated both at baseline and after osmotic stimulus. WDT was complicated by development of acute kidney injury. Abdomen ultrasound demonstrated bilateral hydronephrosis, trabeculated bladder and a residual urine volume of 819 cc, in presence of normal kidney size and prostatic gland. A cysto-urethrography showed a sub-stenosis of 35 mm involving the membranous urethral tract. The patient underwent to balloon dilatation and urethrotomy with complete restitutio ad integrum. In our knowledge, this is the first report of idiopathic urethral stricture complicated by NDI in adult. PPS workup requires a global medical evaluation by an endocrinologist. In the suspicion of NDI, urinary tract obstruction should be considered. WDT remains a cornerstone in the differential diagnosis of PPS and the availability of biomarkers including copeptin may simplify the diagnostic process.
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PMID:Idiopathic Urethral Stricture and Nephrogenic Diabetes Insipidus: The Odd Couple. 3151 86