THE MECHANISM OF THE INITIAL NATRIURESIS AFTER TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT

Background & Aims: The pathogenesis of the delayed natriuresis after t ransjugular intrahepatic portosystemic shunt (TIPS) insertion is unkno wn. This was studied to elucidate the mechanism involved. Methods: In 12 patients with cirrhosis and refractory ascites after TIPS, systemic and venal hemodynamics, renal sodium handling, central blood volume, neurohumoral factors, and hepatic function were studied weekly after t he shunt with the patients receiving a diet of 20 mmol sodium/day. Res ults: Two weeks after TIPS, the initial natriuresis (4 +/- 1 to 18 +/- 3 mmol/day; P < 0.05) was associated with significant reductions in c orrected sinusoidal pressure (24.4 +/- 1.8 to 7.5 +/- 0.4 mm Hg; P < 0 .001), proximal renal tubular reabsorption of sodium (P = 0.05), and r enin-angiotensin-aldosterone activity(P < 0.05), but with significant systemic vasodilatation (P < 0.05). At 4 weeks, negative sodium balanc e was achieved (52 +/- 21 mmol/day; P < 0.01), despite continued syste mic arterial vasodilatation, associated with significant increases in total central and cardiac volumes (P < 0.05) and normalization of seru m aldosterone levels (P < 0.01). Four late responders were significant ly older (P = 0.01) and had significantly lower baseline glomerular fi ltration rates (P = 0.02). Conclusions: In cirrhosis, sinusoidal porta l hypertension and an activated renin-angiotensin-aldosterone system s eem to be important in the pathogenesis of sodium retention. Systemic vasodilatation without arterial underfilling does not prevent natriure sis. Delayed natriuresis after TIPS is associated with increasing age and pre-TIPS renal impairment.