Abstract
Peripheral venous renin activity was determined by the method of Boucher in 15 patients with cirrhosis of the liver and ascites who were on an unrestricted sodium intake. Positive sodium balance was present in all subjects. Marked elevation of mean plasma renin activity (43 ng angiotensin II/min per liter, SD±38) was present. The mean plasma renin activity in 16 normal ambulatory subjects on an unrestricted sodium intake was 10.7 ng (SD±4.9) of angiotensin II/min per liter. The difference was highly significant, P < 0.01. A zero-order enzyme reaction occurred in all but 1 patient; the first-order enzyme reaction in this 1 patient suggests a low renin-substrate concentration in liver disease. The renin-substrate concentration was determined in 18 patients with liver disease (13 with cirrhosis and 5 with hepatitis) and in 10 normal subjects. The renin substrate was expressed in equivalents of angiotensin II formed/100 ml plasma. The mean renin substrate in 13 patients with cirrhosis and ascites was 17,193 ng (SD±6556); the normal mean renin substrate was 34,385 ng (SD ± 5,679), P < 0.01. The lowest renin substrate concentration was seen in 2 patients with severe hepatitis.