Vasopressin excess and hyponatremia

Am J Kidney Dis. 2006 May;47(5):727-37. doi: 10.1053/j.ajkd.2006.01.020.

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.

Publication types

  • Review

MeSH terms

  • Arginine Vasopressin / antagonists & inhibitors*
  • Arginine Vasopressin / physiology*
  • Azepines / therapeutic use
  • Benzamides / therapeutic use
  • Benzazepines / therapeutic use
  • Humans
  • Hyponatremia / drug therapy*
  • Hyponatremia / etiology*
  • Pyrroles
  • Receptors, Vasopressin / metabolism
  • Tolvaptan
  • Water-Electrolyte Balance

Substances

  • Azepines
  • Benzamides
  • Benzazepines
  • Pyrroles
  • Receptors, Vasopressin
  • conivaptan
  • Arginine Vasopressin
  • Tolvaptan
  • lixivaptan