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)

A prospective study was undertaken to define the clinical features, natural history and etiology of post-obstructive diuresis. Studied in detail were 8 patients with a massive diuresis after relief of urinary tract obstruction. We found that urea mediated osmotic diuresis, natriuresis owing to elimination of retained sodium from the obstructed phase, tubular defects in sodium reabsorption, renal unresponsiveness to antidiuretic hormone and iatrogenic factors may play varying roles in each individual diuresis. Overzealous fluid replacement should be avoided.
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PMID:Post-obstructive diuresis: a varied syndrome. 111 14

Postobstructive diuresis occurs after relief of bilateral ureteral obstruction despite the persistent decrease in renal cortical perfusion and glomerular filtration rate (GFR). After an initial transient rise in renal blood flow (RBF) during acute ureteral obstruction, tubular damage and progressive vasoconstriction with decreased RBF, especially of medullary perfusion, are observed with chronic obstruction. These are associated with an activation of the renin-angiotensin system and of renal prostaglandin (PG) synthesis with enhanced production of the vasoconstrictor thromboxane A2. Azotemia and extracellular fluid volume (ECFV) expansion result from impaired renal function. Mechanisms of polyuria following relief from bilateral chronic obstruction include enhanced PGE-mediated medullary blood flow, structural and functional tubular damage with decreased sodium reabsorption and (vasopressin-resistant) impaired renal concentrating ability, osmotic diuresis, activation of natriuretic factors following ECFV-expansion, and sometimes iatrogenic excessive fluid replacement. The resulting loss of fluid and electrolytes represents a major hazard in patients after surgical correction of congenital or acquired urinary tract obstruction.
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PMID:[Mechanisms of postobstructive polyuria]. 293 1

Severe hypernatremia and hyperosmolar dehydration developed in a patient with partial urinary tract obstruction. The urine was initially hypotonic, and there was no response to exogenous vasopressin. These abnormalities resolved with relief of the urinary tract obstruction and replacement of the water deficit. This case documents lower urinary tract obstruction as a cause of nephrogenic diabetes insipidus and severe hypernatremia and illustrates its reversible nature.
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PMID:Severe hypernatremia complicating urinary tract obstruction. 618 76

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) secondary to chronic urinary tract obstruction is a rare condition. The exact cause is unknown; it is likely that increased collecting duct pressures cause damage to the tubular epithelium, resulting in insensitivity to the antidiuretic hormone (ADH). We report a case of NDI associated with ureteral obstruction caused by advanced stage ovarian carcioma in a 20-year-old girl. After debulcking surgery, massive polyuria continued. Several administrations of an ADH analog were ineffective in reducing urine output, suggesting a possible relationship of massive polyuria with NDI. Following oral administration of a thiazide diuretic, known to exert antidiuretic action in NDI, the urine output was dramatically reduced. This case suggests that ureteral obstruction due to ovarian mass may cause NDI and after the surgery thiazide diuretics are effective in reducing urine output in NDI with ureteral obstruction.
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PMID:A case of nephrogenic diabetes insipidus caused by partial bilateral ureteral obstruction due to advanced stage ovarian carcinoma. 1922 93

Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with dilutional hyponatremia (syndrome of inappropriate antidiuresis, congestive heart failure, cirrhosis). Normal regulation of AQP2 by vasopressin involves 2 independent regulatory mechanisms: (1) short-term regulation of AQP2 trafficking to and from the apical plasma membrane, and (2) long-term regulation of the total abundance of the AQP2 protein in the cells. Most disorders of water balance are the result of dysregulation of processes that regulate the total abundance of AQP2 in collecting duct cells. In general, the level of AQP2 in a collecting duct cell is determined by a balance between production via translation of AQP2 mRNA and removal via degradation or secretion into the urine in exosomes. AQP2 abundance increases in response to vasopressin chiefly due to increased translation subsequent to increases in AQP2 mRNA. Vasopressin-mediated regulation of AQP2 gene transcription is poorly understood, although several transcription factor-binding elements in the 5' flanking region of the AQP2 gene have been identified, and candidate transcription factors corresponding to these elements have been discovered in proteomics studies. Here, we review progress in this area and discuss elements of vasopressin signaling in the collecting duct that may impinge on regulation of AQP2 in health and in the context of examples of polyuric diseases.
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PMID:Aquaporin-2 regulation in health and disease. 2313 Sep 44

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