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.
BACKGROUND
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.


OBJECTIVE
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.


METHODS
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.


RESULTS
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.
Wong
Florence
F
Division of Gastroenterology, Department of Medicine, University of Toronto, 9N/983 Toronto General Hospital, 200 Elizabeth Street, Toronto M5G 2C4, Ontario, Canada. florence.wong@utoronto.ca
Raina
Nilima
N
Richardson
Robert
R
D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006530:Hepatorenal Syndrome / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D008099:Liver / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000150:complications*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D012079:Renal Circulation / Q000502:physiology; D012083:Renin / Q000097:blood; D016060:Sorption Detoxification / Q000379:methods*; D017211:Treatment Failure; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D014662:Vasoconstrictor Agents; D000450:Aldosterone; D012083:Renin