Dilutional Hyponatremia in Patients With Cirrhosis and Ascites

Abstract

AN ACTIVATION of the renin-angiotensin-aldosterone system and the sympathetic nervous system and a nonosmotic release of vasopressin frequently develop in patients with cirrhosis. This sequence of events results in enhanced renal water and sodium retention, ascites, impaired free-water excretion, and, frequently, hepatorenal syndrome.^1,2 Hepatorenal syndrome is characterized by a marked reduction in renal blood flow and glomerular filtration rate in the absence of histological abnormalities in the kidney and other known causes of renal failure. It is associated with an extremely short survival.³ Decreased liver size, increased plasma renin activity (PRA), and dilutional hyponatremia have been considered predictors of hepatorenal syndrome in these patients.^3,4 Precipitating factors of hepatorenal syndrome have been described, eg, gastrointestinal tract hemorrhage or bacterial infections.^4,5