Plasma renin activity and renin-substrate concentration in patients with liver disease.

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 (S D ± 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 angio-tensin II formed/100 ml plasma. The mean renin substrate in 13 patients with cirrhosis and ascites was 17,193 ng (S D ± 6 5 5 6) ; the normal mean renin sub-strate was 34,385 ng (SD ± 5,679), P<0.01. The lowest renin substrate concentration was seen in 2 patients with severe hepatitis. ADDITIONAL KEY WORDS hepatitis angiotensin II cirrhosis of the liver atitis angiotensinogen • Many factors have been shown to be important in the pathogenesis of ascites. In cirrhosis of the liver, the scarring process leads to an intrahepatic and portal venous hydrostatic pressure resulting in transudation of fluid into the peritoneal cavity (1). This removal of fluid from the intravascular volume results in stimulation of the juxtaglomer-ular apparatus of the kidney which increases its secretion of renin. This enzyme interacts with angiotensinogen to form angiotensin I, which in turn is acted upon by a converting enzyme to produce angiotensin II. Angioten-sin II has been shown to be the primary controller of the rate of aldosterone secretion (2-5). Aldosterone secretion rate and excretion are increased in patients with cirrhosis of the liver with sodium retention and ascites formation (6, 7). Renin activity was elevated in a few patients studied (8). The present study was undertaken to evaluate more fully the renin-angiotensin system in patients retaining sodium due to cirrhosis of the liver and ascites formation. The renin activity and angioten-sinogen concentration were studied in a group of untreated patients with sodium retention due to cirrhosis of the liver and ascites formation. Angiotensinogen concentration was …