Abstract
Hepatorenal syndrome (HRS) is a pre-renal azotemia-like acute renal failure occurring in patients with end-stage cirrhosis. HRS results from arteriolar vasodilatation, arteriolar underfilling, and intense renal vasoconstriction. By definition, it is not responsive to volume expansion, and the prognosis is especially poor even with the use of terlipressin or albumin dialysis or both. It may be difficult, on the basis of the current criteria, to clearly differentiate HRS from other causes of acute renal failure in cirrhosis. In addition, patients with HRS frequently have underlying chronic kidney changes that may not be reversible after transplantation. In the previous issue of Critical Care, a group of experts proposed a new classification of acute, acute-on-chronic, or chronic renal impairment in cirrhosis on the basis of the RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria. The group proposed the term 'hepatorenal disorder' to define patients with advanced cirrhosis and kidney dysfunction at an earlier stage, regardless of the mechanisms. As stated by the authors, more data are needed to clearly identify, by non-invasive means, those with a potential for improvement with liver transplantation and those who can undergo a combined liver and kidney transplantation.
Highlights
Hepatorenal syndrome (HRS) is a pre-renal azotemialike acute renal failure occurring in patients with end-stage cirrhosis
Cirrhosis is characterized by circulatory changes corresponding to a hyperkinetic state with arterial vasodilatation, decreased systemic vascular resistance, and increased cardiac output [1]
A first set of criteria had been proposed in the mid-’90s to better differentiate HRS from other causes of acute renal failure in cirrhosis, the absence of improvement with volume expansion being central in the definition of HRS [5]
Summary
Hepatorenal syndrome (HRS) is a pre-renal azotemialike acute renal failure occurring in patients with end-stage cirrhosis. A first set of criteria had been proposed in the mid-’90s to better differentiate HRS from other causes of acute renal failure in cirrhosis, the absence of improvement with volume expansion being central in the definition of HRS [5]. It has been shown that a substantial proportion of patients who are undergoing transjugular renal biopsy and who have a clinical diagnosis of HRS do have intrinsic kidney changes, especially tubulointerstitial injury resulting from either comorbidities or chronic ischemia [7].
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