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Hepatorenal syndrome (HRS) is a serious complication of end-stage liver disease, occurring mainly in patients with advanced cirrhosis and ascites, who have marked circulatory dysfunction,1 as well as in patients with acute liver failure.2 In spite of its functional nature, HRS is associated with a poor prognosis,3 4 and the only effective treatment is liver transplantation. During the 56th Meeting of the American Association for the Study of Liver Diseases, the International Ascites Club held a Focused Study Group (FSG) on HRS for the purpose of reporting the results of an international workshop and to reach a consensus on a new definition, criteria for diagnosis and recommendations on HRS treatment. A similar workshop was held in Chicago in 1994 in which standardised nomenclature and diagnostic criteria for refractory ascites and HRS were established.5 The introduction of innovative treatments and improvements in our understanding of the pathogenesis of HRS during the previous decade led to an increasing need to undertake a new consensus meeting. This paper reports the scientific rationale behind the new definitions and recommendations. The international workshop included four issues debated by four panels of experts (see Acknowledgements). The issues were: (1) evidence-based HRS pathogenesis; (2) treatment of HRS using vasoconstrictors; (3) other HRS treatments using transjugular intrahepatic portosystemic stent-shunt (TIPS) and extracorporeal albumin dialysis (ECAD); and (4) new definitions and diagnostic criteria for HRS and recommendations for its treatment.

Measurements of electrical potential difference (pd) and of absorption by a dialysis method were carried out in the terminal ileum of patients with an ileostomy. The pd measured with saline in the lumen and at a few centimetres within the stoma averaged 9.2 mV, lumen negatively charged. The pd values were similar whether the ileostomy had been recently or long established. The pd rose considerably when glucose was added to the luminal solution, the maximum effect being attained with a concentration of 40 mmol/1. With a saline bicarbonate solution (Na 145 or 140 m-equiv/1, K 5, or 10 m-equiv/1) in the dialysis tube, considerable absorption of fluid and sodium was demonstrable with little change in sodium concentration. Potassium secretion occurred with the lower, and absorption with the higher, concentration. The final luminal potassium concentration reached was consistent with a passive distribution between blood and lumen.