Published online Mar 21, 2015. doi: 10.3748/wjg.v21.i11.3197
Peer-review started: October 21, 2014
First decision: November 14, 2014
Revised: December 2, 2014
Accepted: January 30, 2015
Article in press: January 30, 2015
Published online: March 21, 2015
Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. The development of ascites in patients with cirrhosis is multi-factorial. Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone (ADH). The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume resulting in the development of ascites. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and ascites leads to impairment of the kidneys to eliminate solute- free water. This leads to additional compensatory mechanisms including non-osmotic secretion of ADH, also known as arginine vasopressin, further worsening excess water retention and thereby hyponatremia. Hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis, and is an important prognostic marker both before and after liver transplant. The management of hyponatremia in this setting is a challenge as conventional therapy for hyponatremia including fluid restriction and loop diuretics are frequently inefficacious. In this review, we discuss the pathophysiology and various treatment modalities, including selective vasopressin receptor antagonists, for the management of hyponatremia in patients with cirrhosis.
Core tip: Hyponatremia is the most common electrolyte abnormality observed in hospitalized patients and is a common finding in patients with advanced cirrhosis. The management of hyponatremia in cirrhosis is challenging as conventional therapy for hyponatremia including fluid restriction and loop diuretics are frequently inefficacious. Vaptans, drugs that selectively antagonizes the effects of arginine vasopressin on the V2 receptors in the kidney tubules, represent a logical step in the treatment of hyponatremia. The currently available vaptans, however, are not approved for use in patients with cirrhosis due to the increased risk for hepatic failure and mortality.