Gastroenterology/Hepatology Division, Indiana University School of Medicine, 975 W. Walnut, IB 327, Indianapolis, IN, 46202-5121, USA, firstname.lastname@example.org.
The burden of liver disease continues to increase in the United States, with the epidemics of hepatitis C, alcoholic liver disease, and the coming wave of nonalcoholic fatty liver disease patients all contributing to a high burden of individuals with end-stage liver disease. The complications of cirrhosis have been related to portal hypertension or synthetic dysfunction with variceal bleeding, ascites, hepatic encephalopathy, jaundice, hepatorenal syndrome, and the pulmonary complications of cirrhosis being described classically. Over the past decade, a body of evidence has now been assembled demonstrating that hyponatremia is also an important complication in patients with decompensated cirrhosis, with recent data demonstrating that hyponatremia is an important prognostic indicator in those with cirrhosis [1••]. Seminal research has demonstrated the pathophysiologic role of the hyperdynamic circulation and vasodilation in those with decompensated cirrhosis that leads to many of the complications, including hyponatremia [2•]. Moreover, a new class of drugs, the vaptans, have provided important insights into the pathophysiology and potential therapy of those with hyponatremia and possibly in those with hyponatremia and cirrhotic ascites . However, there are safety concerns with some drugs in this class. In this article, the pathophysiology of hyponatremia, clinical relevance to patients with decompensated cirrhosis, and management options will be addressed.