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

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 specialised form of dialysis that clears albumin-bound substances, including vasodilators, and therefore can potentially reduce systemic vasodilatation in cirrhosis.

In patients with cirrhosis, refractory ascites and type 1 HRS not responding to vasoconstrictor treatment, MARS is ineffective in improving systemic haemodynamics 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.

A pilot study was carried out in an academic teaching hospital. The study group comprised six patients with cirrhosis, refractory ascites and type 1 HRS not responding to vasoconstrictor treatment. All patients received 5 days of 6-8 h of MARS dialysis. The main outcome measures were pre-MARS and post-MARS measurements of glomerular filtration rate, renal blood flow, neurohormones, cytokines and nitric oxide (NO), as well as daily biochemistry, haematology and urinary volume.

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

There were no significant changes in systemic haemodynamics and GFR following MARS treatments, despite a significant reduction in NO concentrations (111.5+/-18.8 micromol/l pre-MARS, to 65.1+/-8.2 micromol/l post-MARS, p=0.05). There was a transient reduction in serum creatinine (p<0.05), Child-Pugh and MELD (Model End-Stage Liver Disease) scores with MARS, but no significant difference was observed in neurohormone and cytokine levels. Four of six patients died following MARS treatments. Conclusions: In patients with cirrhosis, refractory ascites and type 1 HRS not responding to vasoconstrictor treatment, MARS is ineffective in improving systemic haemodynamics 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.