Renin-Aldosterone Axis in Refractory Hepatic Ascites. Characterization of The Response of the Axis to Both the Acute and Long Term Effects of Peritoneuvenous Shunting

Abstract

Twenty-two patients with refractory asc1tes secondary to chronic liver disease undergoing pcritoneovenous shunting (PVS) were studied under strict metabolic conditio ns, preoperatively and for the fir st 8 h postoperatively. Fourtren subjects were restudied under si milar metabolic conditions three months post-l 1 VS. Thirteen of the 22 patients (59%) had an immediate dramatic natriuresis and entered negative sodium balance (group A), the remaining nine patients !41.,.o) remained in positive sodium balance during the first 8 h post-PVS (group B) Group B was characteri zed preoperatively by significantly higher mean plasma rcnin activity (P· 0.01) and scrum aldosterone levels (P, 0.01) compared to group A Yet, plasma renin activity and aldosterone levels in both groups were similar at 8 h following shunting. At three mo nths post-PVS in the 14 patients restudied, mean plasma renin activity and seru m aldosterone levels were not significantly elevated above the normal range. Yet the patients still demonstrated continued sodium retention on a 20 mEq sodium diet, mean sodium excretion 10.5 ± 2.8 mEq/day. The close correlation of sc rum aldosteronc with plasma renin activity and the parallel suppressio n acutely post-PVS, indicate that the level of plasma renin activity is a major determinant of serum aldosterone in re fractory ascites. However, the find ing of normal preoperative values for plasma renin acti vity and aldosterone in certai n patients, combined with the failure of group B subjects to enter negative sodium balance despite acute normalization of aldosterone, would indicate that fa ctors other than activation of the renin-aldosterone axis contrib­ ute to the sodium retention of chronic liver disease. This conclusion is supported by the late results which document persistent sodium retentio n three months following PVS, despite normalization of aldosterone and presumably normaliza­ tion of any deficit in effective plasma volume. Can J Gastroenterol 1989;3(3): 103·110 (Pour resume voir page 104)