ABSTRACT
Derangements in fluid and electrolyte balance and renal function commonly occur in
the natural history of cirrhosis. Renal abnormalities occur in the setting of a
hyperdynamic state characterized by an increased cardiac output, a reduction in total
vascular resistance and an activation of neurohormonal vasoactive systems. This
circulatory dysfunction, a consequence of intense arterial vasodilation in the splanchnic
circulation, is considered a primary feature in the pathogenesis of sodium and water
retention in cirrhosis. Sodium retention is the first and main factor involved in the
formation of ascites and edema in patients with cirrhosis. The principal event
responsible for local splanchnic vasodilation seems to be the overproduction of nitric
oxide (NO). Splanchnic vasodilation by decreasing effective arterial blood volume causes
homeostatic activation of vasoconstrictor and antinatriuretic factors triggered to
compensate for a relative arterial underfilling. The net effect is avid retention of sodium
and water as well as renal vasoconstriction in advanced stages. The mechanisms of ascites
formation and sodium and water retention in patients with cirrhosis are discussed in
this chapter.
