The aim of this study was to determine whether liver function and portoeystemic shunting are related to renal sodium retention in alcoholic liver disease. Twenty-three studies were performed; 10 patients had ascites. Liver function was assessed from the plasma elimination rates of antipyrine, caffeine and stable isotopes of cholic acid, the latter administered both orally [2,2,4,4-2β¬il and intravenously l24-13CI. Porto- SyBtemic shunt fraction was calculated as the ratio of the intravenous and oral clearances of the isotopes of cholic acid.
Portosystemic shunt fraction waa similar in patients with and without ascites (61% * 16% vs. 64% f 11%) and unrelated to urinary sodium excretion in patients with ascites (r = -0.146). Patients with ascites had significantly lower elimination rates of all administered compounds aa compared with patients without ascites (antipyrine = 0.012 * 0.007 vs. 0.031 f O.O16/hr, p < 0.001; caffeine = 0.014 * 0.013 vs. 0.061 f O.O41/hr, p < 0.002; intravenous cholic acid = 1.365 f 0.442 vs. 2.284 f O.WS/hr, p = 0.006; red cholic acid = 2.178 * 0.841 vs.
orally arlmlnlntc?
4.058 * 1.837/hr, p = 0.007). However, urinary d u m excretion in patients with ascites was not related to the elimination constants of these compounds (r = 0.360, 0.319,0.067, -0.073, respectively). Ascites complicating alcoholic liver disease is aesociated with impaired liver function but not the extent of portoeyetemic shunting. (HEPATOLOGY 1990,12:466-469.) . .
The pathogenesis of sodium retention complicating chronic liver disease is unsettled (1). Portosystemic shunting and liver function might mediate renal sodium retention by permitting increased systemic availability of a compound with an effect on renal sodium handling. However, the interrelationships between portosystemic