Renal failure in the patient with cirrhosis: The role of active vasoconstriction

Abstract

Renal hemodynamics were studied with the ¹³³Xe washout technic and renal arteriography in fifteen patients with cirrhosis and varying degrees of renal functional impairment. In cirrhotic patients with renal failure extreme hemodynamic instability was encountered, characterized by variability and irregularity of xenon washout, in contrast to patients with renal failure of other etiology. Marked instability was more frequent in cirrhotic patients with azotemia, and was so severe in three instances that the curves were unanalyzable. The remaining curves revealed a decrease in both mean renal blood flow and the percentage of flow in the rapid flow component in approximate proportion to the decrease in creatinine clearance, suggesting a reduction in cortical perfusion. The arteriographic findings, including the absence of a cortical nephrogram and unrecognizable renal cortical vasculature in the patients with the most severe degree of renal failure, support the concept of a reduction in renal cortical perfusion. The finding of marked hemodynamic instability strongly suggests that the renal ischemia is secondary to active vasoconstriction. Consistent reversal of all the vascular abnormalities in the kidneys of five cirrhotic patients at postmortem angiography provides further evidence for the functional basis of the renal failure, operating through active renal vasoconstriction. Phentolamine infusion into the renal artery in four patients did not significantly alter renal hemodynamics indicating that increased sympathetic nervous system activity was not responsible for the active vasoconstriction and cortical ischemia.