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 total of 29 patients with severe hemorrhagic fever associated with the renal syndrome were studied for impact of extracorporeal hemodialysis on the activity of the renin-aldosterone system (RAS), plasma vasopressin and osmolality and the levels of the major osmotically active agents, as well as the circadian urine output and blood pressures. In patients with oliguria there was a significant activation of RAS, an increase in plasma vasopressin ad osmolality due to the increment of the urea in presence of hyponatremia. Hemodialysis led to a temporary normalization of plasma aldosterone and vasopressin levels and a decrease in blood pressure. No significant changes were documented in the activity of the plasma renin and circadian urinary output. A direct correlation was established between the plasma osmolality and the levels of vasopressin. In patients with polyuria developed in presence of hypernatremic hyperosmia plasma vasopressin elevated and aldosterone dropped.
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PMID:[The effect of hemodialysis on the vasopressin level and on the renin-aldosterone system in patients with hemorrhagic fever with renal syndrome]. 197 Sep 14

Changes in blood plasma content of hormones which are observed in the different periods of hemorrhagic fever and the attendant renal syndrome are directed to the maintenance of significantly deranged water-electrolyte homeostasis. Adequate secretion of vasopressin and aldosterone in response to the changes in sodium concentration and plasma osmolality point to the absence of significant functional disorders of the corresponding glands. Pronounced hypernatremia in fatal cases is evidence of the deranged processes of osmoregulation associated primarily with kidney areactivity to vasopressin and prognostically is an unfavourable sign. The presence of pituitary necrosis in deceased subjects does not rule out the role of vasopressin deficiency in the pathogenesis of pronounced hypernatremia.
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PMID:[Pathogenesis of water-electrolyte imbalance in acute renal failure in patients with hemorrhagic fever with nephrotic syndrome]. 256 11

To evaluate renal tubular functions and to investigate the causative factors of urinary-concentrating defects in the late stage of hemorrhagic fever with renal syndrome (HFRS), 11 HFRS patients in the convalescent phase were studied and compared with 8 acute renal failure (ARF) patients in convalescence (disease controls) and 9 healthy adults preparing for kidney donation (normal controls, NC). Minimal urine osmolality induced by water loading was higher (p < 0.05) in HFRS (89.5 +/- 22.1 mosm/kg) and ARF patients (84.8 +/- 14.7 mosm/ kg) than in NC (47.8 +/- 4.6 mosm/kg), but the solute-free water clearance of HFRS patients (9.0 +/- 1.3%), measured at maximal diuresis, was not different from that of ARF patients (6.7 +/- 1.2%) or NC (10.5 +/- 1.4%). After 12-hour water deprivation + vasopressin stimulation, HFRS had lower urine osmolality (433.7 +/- 31.1 versus 850.0 +/- 35.1 mosm/kg; p < 0.05), urine-to-plasma osmolality ratio (1.47 +/- 0.11 versus 2.91 +/- 0.11; p < 0.05), and solute-free water reabsorption (0.53 +/- 0.07 versus 0.91 +/- 0.12%; p < 0.05) than NC. As compared with ARF patients (1.09 +/- 0.16%) or NC (1.49 +/- 0.16%), HFRS patients (0.43 +/- 0.20%) had lower solute-free water reabsorption measured at maximal antidiuresis induced by water deprivation + vasopressin stimulation + hypertonic saline infusion (p < 0.05). In HFRS, the plasma vasopressin level and plasma vasopressin/osmolality ratio increased from 3.9 +/- 0.8 to 6.1 +/- 1.1 pg/ml and from 0.013 +/- 0.003 to 0.020 +/- 0.004 pg/ml/mosm/kg after 12-hour water deprivation, respectively (p < 0.01). However, neither basal nor stimulated values of the plasma vasopressin level or plasma vasopressin/osmolality ratio was different among the 3 groups. HFRS patients were not different from ARF patients or NC in lithium clearance, urinary-acidifying capacity, and fractional excretions of sodium, potassium and bicarbonate. We conclude that in the convalescent phase of HFRS, the urinary-acidifying ability is not disturbed, the urinary-diluting defect is mild, and the urinary-concentrating capacity is obviously impaired. This study suggests that the most important factor contributing to the urinary-concentrating defect in HFRS is the reduced collecting duct responsiveness to vasopressin.
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PMID:Evaluation of renal tubular functions in convalescent phase of hemorrhagic fever with renal syndrome. 1064 33