Hepatorenal Syndrome: Is It the Magnitude of the Renal Failure that Matters?

Abstract

To the Editor: Hepatorenal syndrome (HRS) is a serious and life threatening complication of end stage liver disease and the criteria for its diagnosis were defined in 1996 [1] and revisited in 2007 [2]. The first definition was a set of major and minor criteria where the renal function was considered abnormal if the creatinine was[1.5 mg/dL or the creatinine clearance was\40 mL/min. The new consensus considered impaired renal function as having a creatinine value [1.5 mg/dL without improvement after 48 h of diuretic withdrawal and volume expansion with intravenous albumin [1, 2]. Neither of these definitions takes into account the magnitude of the rise in creatinine and its association with the reversibility or prognosis of hepatorenal syndrome. In January 2012, our group published in this journal [3] the largest series of patients with HRS type 1 in the last 5 years according to the new Ascites Club definition of this disease. We described the etiology of the end stage liver disease (ESLD) and the serum creatinine as independent predictive factors for survival in HRS. In 2011, Boyer et al. [4] also published their work regarding response of HRS to treatment with terlipressin versus placebo, finding that serum creatinine is a prognostic factor for survival and HRS reversal, while MELD score and bilirubin did not have an independent prognostic value, confirming our results and even considering that serum creatinine might be the best predictor of HRS reversal. The same finding has been documented by Martin-Llahi et al. [5] in a study comparing terlipressin plus albumin with albumin alone in the reversal of HRS. What makes our results even more interesting, is the fact that terlipressin, considered in Europe and Latin America the standard of care for HRS, was not used in our population (we used midodrine and octreotide) and creatinine continues to be an independent strong prognostic factor for patient survival and HRS reversal. In the paper of Boyer et al. [4] it is emphasized that neither MELD score nor bilirubin are independent predictors of survival. This leaves again the creatinine level as the sole predictor of reversibility and survival. There are several questions to be answered regarding HRS and its prognosis: should we consider the creatinine level as the only variable prognosticating outcome? Is there a creatinine level at which treatment is futile? Is early treatment during HRS justified? Should we adopt terlipressin as our standard of treatment? Is terlipressin better than midodrine and octreotide? What is obvious is that HRS is a multisystem disease, recently re-defined, which might require further panel discussion, and probably the Ascites Club should have meetings during national and international conferences at regular intervals.