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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.

The CLIF-C ACLFs at ACLF diagnosis is superior to the MELDs and MELD-Nas in predicting mortality. The CLIF-C ACLFs is a clinically relevant, validated scoring system that can be used sequentially to stratify the risk of mortality in ACLF patients.

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During the last decade great advances have been made of water retention and dilutional hyponatremia in human cirrhosis. Finally, the field of spontaneous infection of concerning the pathogenesis and treatment of ascites. A new hypothesis on the mechanism of renal dysfunction ascitic fluid (spontaneous bacterial peritonitis) is also experiencing major changes. The demonstration of intestiand ascites formation in cirrhosis has been proposed 1 and this has greatly stimulated research in this area. The nal bacterial translocation in experimental models of cirrhosis, 12 the potential role of cytokines in some discovery of the important role played by the vascular endothelium in the homeostasis of systemic hemodynam-complications associated with this infection, 13 the identification of subgroups of cirrhotic patients predisposed to ics and renal function 2,3 has also opened an important field of research into pathophysiology, and evidence has develop spontaneous bacterial peritonitis, 14 and the effectiveness of selective intestinal decontamination in the been presented implicating endothelial factors in the pathogenesis of systemic circulatory dysfunction in cir-primary and secondary prophylaxis of spontaneous bacterial peritonitis 15,16 are the most relevant developments. rhosis 4,5 and hepatorenal syndrome (HRS). 6 The reintroduction of therapeutic paracentesis has greatly modifiedIn clear contrast to these advances, little attention has been paid to the standardization of the nomenclathe treatment of cirrhotic patients with tense or refractory ascites. 7 The transjugular intrahepatic portosys-ture and diagnostic criteria of different syndromes associated with ascites in cirrhosis. The existence of a temic shunt is another therapeutic tool of potential interest in the management of refractory ascites. 8 The uniform language, however, is essential in modern medicine. It facilitates communication among clinisynthesis of orally-active specific antagonists of the tubular effect of antidiuretic hormone and inhibitors of antidi-cians and researchers and ensures unambiguous diagnoses and more confident prognoses. Moreover, it uretic hormone release will probably add new drugs to the pharmacological armamentarium for patients with improves pathophysiological and therapeutic investigations, simplifies the analysis of therapeutic trials, cirrhosis and ascites. These ''aquaretic drugs,'' which normalize renal water metabolism in experimental cirrhosis and stimulates multicenter studies. and ascites, 9-11 are of potential interest for the treatment PREVIOUS CONSENSUS DEFINITIONS OF HEPATORENAL SYNDROME AND

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Acute‐on‐chronic liver failure (ACLF) is characterized by acute decompensation (AD) of cirrhosis, organ failure(s), and high 28‐day mortality. We investigated whether assessments of patients at specific time points predicted their need for liver transplantation (LT) or the potential futility of their care. We assessed clinical courses of 388 patients who had ACLF at enrollment, from February through September 2011, or during early (28‐day) follow‐up of the prospective multicenter European Chronic Liver Failure (CLIF) ACLF in Cirrhosis study. We assessed ACLF grades at different time points to define disease resolution, improvement, worsening, or steady or fluctuating course. ACLF resolved or improved in 49.2%, had a steady or fluctuating course in 30.4%, and worsened in 20.4%. The 28‐day transplant‐free mortality was low‐to‐moderate (6%‐18%) in patients with nonsevere early course (final no ACLF or ACLF‐1) and high‐to‐very high (42%‐92%) in those with severe early course (final ACLF‐2 or ‐3) independently of initial grades. Independent predictors of course severity were CLIF Consortium ACLF score (CLIF‐C ACLFs) and presence of liver failure (total bilirubin ≥12 mg/dL) at ACLF diagnosis. Eighty‐one percent had their final ACLF grade at 1 week, resulting in accurate prediction of short‐ (28‐day) and mid‐term (90‐day) mortality by ACLF grade at 3‐7 days. Among patients that underwent early LT, 75% survived for at least 1 year. Among patients with ≥4 organ failures, or CLIF‐C ACLFs >64 at days 3‐7 days, and did not undergo LT, mortality was 100% by 28 days. Conclusions: Assessment of ACLF patients at 3‐7 days of the syndrome provides a tool to define the emergency of LT and a rational basis for intensive care discontinuation owing to futility. (Hepatology 2015;62:243‐252)

These data support SI as the primary driver of ACLF in cirrhosis. (Hepatology 2016;64:1249-1264).