Organ interactions in the hepatorenal syndrome

An increasing number of patients with severe liver dysfunction are admitted to the ICU for stabilization and organ-specific support, including liver transplantation. Global impairment of hepatic performance frequently results in pathologic organ interactions that limit the potential for recovery. One of the most notable of these interactions is the hepatorenal syndrome, an otherwise uniformly fatal complication of end-stage liver disease characterized by the progressive development of oliguria and low urine sodium excretion. The syndrome can occur in the setting of either acute or chronic liver disease, and portal hypertension may be important in the pathogenesis. The patient with the hepatorenal syndrome also has a number of systemic circulatory abnormalities induced by liver disease and/or portal hypertension, but the exact pathologic role of these abnormalities in the development of oliguria is uncertain. It is reasonably well established that diminished systemic BP characteristic of liver failure is not the primary cause of renal insufficiency. Rather, intrarenal preglomerular vasoconstriction mediated by unknown stimuli is the major defect in the hepatorenal syndrome, manifested by relative ischemia. Current data point to abnormal renal sympathetic innervation as one of the more likely major causes of this vasoconstriction. After exclusion of systemic intravascular volume depletion and other causes of oliguria, dialytic therapy is indicated when liver transplantation or recovery of liver function is anticipated; terminal supportive care is appropriate when these outcomes are not options.