Splanchnic and hepatic renin metabolism in alcoholic cirrhosis. Lack of evidence of a splanchnic source of production or of significantly impaired hepatic clearance.

Cirrhosis is frequently associated with increased arterial plasma renin activity. This could be the result of increased renin production or diminished renin clearance. We measured plasma renin activity in simultaneous portal, hepatic vein, and femoral artery blood samples in 7 patients with clinically stable alcoholic cirrhosis to determine whether hepatic extraction of renin is reduced and whether, as has been suggested, there is a splanchnic source of plasma renin activity in this condition. Plasma renin activity (mean +/- S.E. in ng/ml/min) was similar in portal, arterial, and hepatic venous samples (portal: 8.0 +/- 3.7; arterial: 7.6 +/- 3.1; hepatic vein: 6.4 +/- 2.3). Hepatic extraction of plasma renin activity, calculated as [arterial-hepatic vein)/arterial) X 100, was 14 +/- 6%, not significantly different from reported normal values (26 +/- 3%, n = 46). The intrinsic hepatic clearance of plasma renin activity (235 +/- 89 ml/min) and the hepatic renin extraction rate (1.801 +/- 1.032 micrograms/min) were also similar to estimated normal values. The intrinsic clearance and extraction rates of renin correlated with arterial plasma renin activity (r = 0.93, P less than 0.01 and r = 0.79, P less than 0.05). These data indicate that in clinically stable patients with alcoholic cirrhosis: (1) hepatic renin clearance is not significantly impaired; and (2) there is not a splanchnic source of plasma renin activity. Therefore, increased peripheral plasma renin activity in this condition is due solely to increased renal renin production.