Hepatic Diseases



Renal dysfunction associated with liver disease ranges from glomerulopathies, as seen with hep­atitis B, to azotemic syndromes, as seen with cir­rhosis of the liver. The latter conditions usually occur in decompensated cirrhosis associated with an elevated serum bilirubin and ascites. The azo­temia is most often due to a reduction in the ef­fective circulating volume and in renal blood flow. This situation occurs in the face of a reduc­tion in serum albumin and oncotic pressure with third-spacing of extracellular fluids in ascites.
The hepatorenal syndrome is, almost by defi­nition, a terminal event identified by oliguria, a declining GFR, and tremendous renal sodium avidity. The urinary sodium concentration is almost always less than 10 mEq/L, and there is a dispro­portionately high BUN/creatinine ratio in most cases. The decline in renal function usually fol­lows one of three events in a cirrhotic patient with ascites: sepsis, a vigorous attempt to reduce as­cites with diuretics, or a large-volume paracen­tesis. The kidneys are normal as judged from their recovery of function if transplanted into a non-cirrhotic host. It is not known if the functional renal defect is induced by a hepatic toxin.

Ascites and edema in cirrhotic patients repre­sent cosmetic rather than medical problems in most cases. When it is necessary to reduce ascites or edema in these patients, sodium restriction and the sparing use of diuretics are indicated in order to reduce the risk of a decline in renal function. Acute expansion of intravascular volume may re­verse azotemia in some cirrhotic patients. Dialysis is generally not indicated unless there is a rea­sonable expectation of improved hepatic func­tion.