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Vasopressin Excess and Hyponatremia

Authors
Journal
American Journal of Kidney Diseases
0272-6386
Publisher
Elsevier
Publication Date
Volume
47
Issue
5
Identifiers
DOI: 10.1053/j.ajkd.2006.01.020
Keywords
  • Hyponatremia
  • Arginine Vasopressin–Receptor Antagonist
  • Syndrome Of Inappropriate Secretion Of Antidiuretic Hormone
  • Cirrhosis
  • Congestive Heart Failure
Disciplines
  • Biology

Abstract

Hyponatremia is a common electrolyte disorder that frequently is overlooked and undertreated. Although the pathophysiological process of hyponatremia is complex, arginine vasopressin (AVP) is a common etiologic factor. Excess AVP release by osmotic or nonosmotic stimuli or both can lead to sodium and water imbalance. Conventional treatment options for hyponatremia, including water restriction and administration of sodium chloride with or without loop diuretics, do not directly address the underlying water retention induced by excess AVP in many cases. Clinical trials showed that AVP-receptor antagonists, including lixivaptan, tolvaptan, and conivaptan, produce aquaresis, the electrolyte-sparing excretion of free water, to correct serum sodium concentration. We review results from recent clinical trials involving AVP-receptor antagonists in the treatment of hyponatremia associated with AVP excess.

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