Molecular adsorbent recirculating system is ineffective in the management of type 1 hepatorenal syndrome in cirrhotic patients with ascites who have failed vasoconstrictor therapy

Florence Wing ^1*, Nilima Raina ¹ and Robert Richardson ¹

¹ Toronto General Hospital, Canada

^* To whom correspondence should be addressed. E-mail: florence.wong{at}utoronto.ca.

Accepted 21 July 2009

Abstract

The pathogenetic mechanism of hepatorenal syndrome (HRS) is paradoxical renal vasoconstriction consequent upon systemic and splanchnic arterial vasodilatation. Molecular adsorbent recirculating system (MARS) is a specialized form of dialysis that clears albumin-bound substances, including vasodilators, and therefore can potentially reduce systemic vasodilatation in cirrhosis.

Objective: To assess the efficacy of MARS in improving systemic and renal hemodynamics in cirrhotic patients with refractory ascites and type 1 HRS not responding to vasoconstrictor therapy.

Design: Pilot study.

Setting: Academic teaching hospital.

Patients: Six patients with cirrhosis, refractory ascites and type 1 HRS not responding to vasoconstrictor therapy.

Interventions: All patients received 5 days of 6 to 8 hours of MARS dialysis.

Main outcome measures: Pre- and post- MARS measurements of glomerular filtration rate (GFR), renal blood flow, neurohormones, cytokines and nitric oxide, as well as daily biochemistry, hemotology, and urinary volume were performed.

Results: There were no significant changes in systemic hemodynamics and GFR following MARS treatments, despite significant reduction in nitric oxide (NO) concentrations (111.5 ± 18.8 µmol/L pre-MARS, to 65.1 ± 8.2 µmol/L post-MARS, p=0.05). There was a transient reduction in serum creatinine (p<0.05), Child-Pugh and MELD scores with MARS, but no significant difference was observed in neurohormones and cytokines levels. Four of six patients died following MARS treatments. Conclusions: In patients with cirrhosis, refractory ascites, and type 1 hepatorenal syndrome not responding to vasoconstrictor therapy, MARS is ineffective in improving systemic hemodynamics and renal function despite reduction in NO levels, suggesting that vasodilatation in advanced cirrhosis is not due to excess systemic vasodilators alone. Transient reduction in serum creatinine indicates direct removal by MARS, and may not represent improved renal function.