Abstract
Patients with cirrhosis and ascites are often on the brink of renal failure. Their renal function is vulnerable because of the poorly understood, complex hemodynamic abnormalities that occur in advanced cirrhosis. These abnormalities include an increase in circulating vasodilators, increased cardiac output, low peripheral vascular resistance, and compensatory activation of vasoconstrictor mechanisms.1 The net result of these changes is central hypovolemia, with a consequent progressive reduction in renal perfusion and function. This ultimately leads to the development of the hepatorenal syndrome, which is a severe impairment of renal function in the absence of any identifiable renal structural abnormality.2 The hepatorenal . . .