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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The mechanism of the initial natriuresis after transjugular intrahepatic portosystemic shunt.

BACKGROUND & AIMS: The pathogenesis of the delayed natriuresis after transjugular intrahepatic portosystemic shunt (TIPS) insertion is unknown. This was studied to elucidate the mechanism involved. METHODS: In 12 patients with cirrhosis and refractory ascites after TIPS, systemic and renal hemodynamics, renal sodium handling, central blood volume, neurohumoral factors, and hepatic function were studied weekly after the shunt with the patients receiving a diet of 20 mmol sodium/day. RESULTS: Two weeks after TIPS, the initial natriuresis (4 +/- 1 to 18 +/- 3 mmol/day; P < 0.05) was associated with significant reductions in corrected 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 renin-angiotensin-aldosterone activity (P < 0.05), but with significant systemic vasodilatation (P < 0.05). At 4 weeks, negative sodium balance was achieved (52 +/- 21 mmol/day; P < 0.01), despite continued systemic arterial vasodilatation, associated with significant increases in total central and cardiac volumes (P < 0.05) and normalization of serum aldosterone levels (P < 0.01). Four late responders were significantly older (P = 0.01) and had significantly lower baseline glomerular filtration rates (P = 0.02). CONCLUSIONS: In cirrhosis, sinusoidal portal hypertension and an activated renin-angiotensin-aldosterone system seem to be important in the pathogenesis of sodium retention. Systemic vasodilatation without arterial underfilling does not prevent natriuresis. Delayed natriuresis after TIPS is associated with increasing age and pre-TIPS renal impairment.[1]


  1. The mechanism of the initial natriuresis after transjugular intrahepatic portosystemic shunt. Wong, F., Sniderman, K., Liu, P., Blendis, L. Gastroenterology (1997) [Pubmed]
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