Renal and hemodynamic effects of the peritoneovenous shunt. II. Long-term effects

The long-term renal and hemodynamic effects of the peritoneovenous shunt for intractable ascites were studied in 11 patients to elucidate the mechanism of its persistent beneficial effect. Sodium balance studies were performed in 7 patients. All had patent shunts and no clinically detectable ascites. On a 20-mEq sodium diet, the mean sodium excretion was 17.2 +/- 5.3 mEq/day which was increased over the preoperative mean of 2.4 +/- 0.4 (p < 0.025) on the same diet. There was a 100% increase in creatinine clearance over the preoperative level (p < 0.0005). The mean plasma renin activity and serum aldosterone levels were within normal limits in most patients, and the sodium excretion correlated inversely with the levels of each. During 100-mEq sodium challenge diet, the sodium excretion ranged from 4 to 130 mEq/day with a mean of 56.1 +/- 16.5 and with 6 of the 7 patients displaying sodium retention. On this diet the mean creatinine clearance was 104.3 +/- 6.4 ml/min, and the mean plasma renin activity and serum aldosterone levels had decreased physiologically with the higher sodium intake. Again the sodium excretion correlated inversely with the serum aldosterone on the 100-mEq sodium diet. In 8 patients, the portal pressure, as reflected by the wedge hepatic vein pressure, had decreased by a mean of 37% (p < 0.0005). But, despite this, 2 of the 8 patients had major variceal hemorrhages postoperatively. There was a significant inverse correlation between the increase in sodium excretion and the fall in portal pressure in 4 patients. Thus, sodium retention in cirrhosis is multifactorial with the reninaldosterone system and, possibly, portal hypertension per se both playing a role. Peritoneovenous shunting in carefully selected patients partially reverses the sodium retention and renders patients more manageable over the long term.