title: Managing hyponatremia in patients with heart failure.
abstract: Approximately 20% of heart failure patients have low levels of serum sodium, often at a time when they are hospitalized during a period of decompensation. The presence of hyponatremia adversely affects outcomes in heart failure and is associated with impaired cognitive and neuromuscular function. Current strategies for treating hyponatremia in heart failure patients have limited efficacy. Although the development of hyponatremia in heart failure patients is polyfactorial, the nonosmotic release of arginine vasopressin (AVP) from the posterior pituitary plays a dominant role in this process through its effects on regulating the absorption of free water in the distal portion of the nephron. Drugs which block the effects of AVP on the V2 receptor have been shown to increase serum sodium by promoting the excretion of free water from the kidney. In this review, the theoretical basis supporting the use of AVP blockers is discussed and results from clinical trials in which they were administered to euvolemic and hypervolemic patients are reviewed. Administration of AVP blockers to heart failure patients increases free water excretion, promotes weight loss, and increases serum sodium levels without significant major adverse effects. Clinical trial results demonstrate safety during long-term administration. These findings indicate that the use of AVP receptor antagonists should be considered in heart failure patients who have evidence of significant hyponatremia.
authors.affiliation: Department of Internal Medicine, University of California, San Diego, San Diego, California. bgreenberg@ucsd.edu.
authors.forename: Barry
authors.initials: B
authors.lastname: Greenberg
mesh_terms: D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines / Q000627:therapeutic use; D019468:Disease Management; D006333:Heart Failure / Q000453:epidemiology* / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007010:Hyponatremia / Q000453:epidemiology* / Q000503:physiopathology / Q000628:therapy*; D017483:Receptors, Vasopressin / Q000502:physiology
chemical_list: D065092:Antidiuretic Hormone Receptor Antagonists; D001552:Benzazepines; D017483:Receptors, Vasopressin; C106389:conivaptan