Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites

Abstract

Taurine is a non-protein sulfur aminoacid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostatis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 μmoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginin vasopressine were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340±43 to 817±116 μl/min (p<0.01); urinary sodium from 13.8±3 to 26.3±4 μmoles/min (p<0.05). Both values returned to normal after 2–3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7±2.2 to 4.3±1.9 ng/ml/hr, p<0.05) and aldosterone (from 588±47 to 348±89 pg/ml, p<0.05), but no changes in atrial natriuretic peptide and arginin vasopressine. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.