Afferent mechanisms of sodium retention in cirrhosis and hepatorenal syndrome.

Cirrhosis induces extra-cellular fluid volume expansion, which when the disease is advanced can be severe and poorly responsive to therapy. Prevention and/or effective therapy for cirrhotic edema requires understanding the stimulus that initiates and maintains sodium retention. Despite much study, this stimulus remains unknown. Work over the last several years has shown that signals originating in the liver can influence a variety of systemic functions, including extra-cellular fluid volume control. We review work on the afferent mechanisms triggering sodium retention in cirrhosis and suggest that the data are most consistent with the existence of a sensor in the hepatic circulation that contributes to normal extra-cellular fluid volume control (that is, a 'volume' sensor) and that in cirrhosis, the sensor is pathologically activated by the hepatic circulatory abnormalities caused by the disease. Detailed analysis of the hepatic circulation in normal conditions and cirrhosis is needed.