Hepatorenal syndrome: the 8th international consensus conference of the Acute Dialysis Quality Initiative (ADQI) Group

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Abstract

Introduction

Renal dysfunction is a common complication in patients with end-stage cirrhosis. Since the original publication of the definition and diagnostic criteria for the hepatorenal syndrome (HRS), there have been major advances in our understanding of its pathogenesis. The prognosis of patients with cirrhosis who develop HRS remains poor, with a median survival without liver transplantation of less than six months. However, a number of pharmacological and other therapeutic strategies have now become available which offer the ability to prevent or treat renal dysfunction more effectively in this setting. Accordingly, we sought to review the available evidence, make recommendations and delineate key questions for future studies.

Methods

We undertook a systematic review of the literature using Medline, PubMed and Web of Science, data provided by the Scientific Registry of Transplant Recipients and the bibliographies of key reviews. We determined a list of key questions and convened a two-day consensus conference to develop summary statements via a series of alternating breakout and plenary sessions. In these sessions, we identified supporting evidence and generated recommendations and/or directions for future research.

Results

Of the 30 questions considered, we found inadequate evidence for the majority of questions and our recommendations were mainly based on expert opinion. There was insufficient evidence to grade three questions, but we were able to develop a consensus definition for acute kidney injury in patients with cirrhosis and provide consensus recommendations for future investigations to address key areas of uncertainty.

Conclusions

Despite a paucity of sufficiently powered prospectively randomized trials, we were able to establish an evidence-based appraisal of this field and develop a set of consensus recommendations to standardize care and direct further research for patients with cirrhosis and renal dysfunction.

Related collections

Most cited references 131

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Prediction of Creatinine Clearance from Serum Creatinine

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A formula has been developed to predict creatinine clearance (C cr ) from serum creatinine (S cr ) in adult males: Ccr = (140 – age) (wt kg)/72 × S cr (mg/100ml) (15% less in females). Derivation included the relationship found between age and 24-hour creatinine excretion/kg in 249 patients aged 18–92. Values for C cr were predicted by this formula and four other methods and the results compared with the means of two 24-hour C cr’s measured in 236 patients. The above formula gave a correlation coefficient between predicted and mean measured Ccr·s of 0.83; on average, the difference between predicted and mean measured values was no greater than that between paired clearances. Factors for age and body weight must be included for reasonable prediction.

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Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort study.

Andrea Lassnigg, Daniel Schmidlin, Mohamed Mouhieddine … (2004)

Acute renal failure increases risk of death after cardiac surgery. However, it is not known whether more subtle changes in renal function might have an impact on outcome. Thus, the association between small serum creatinine changes after surgery and mortality, independent of other established perioperative risk indicators, was analyzed. In a prospective cohort study in 4118 patients who underwent cardiac and thoracic aortic surgery, the effect of changes in serum creatinine within 48 h postoperatively on 30-d mortality was analyzed. Cox regression was used to correct for various established demographic preoperative risk indicators, intraoperative parameters, and postoperative complications. In the 2441 patients in whom serum creatinine decreased, early mortality was 2.6% in contrast to 8.9% in patients with increased postoperative serum creatinine values. Patients with large decreases (DeltaCrea or =0.5 mg/dl. For all groups, increases in mortality remained significant in multivariate analyses, including postoperative renal replacement therapy. After cardiac and thoracic aortic surgery, 30-d mortality was lowest in patients with a slight postoperative decrease in serum creatinine. Any even minimal increase or profound decrease of serum creatinine was associated with a substantial decrease in survival.

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Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares.

Paul E Marik, Michael Baram, Bobbak Vahid (2008)

Central venous pressure (CVP) is used almost universally to guide fluid therapy in hospitalized patients. Both historical and recent data suggest that this approach may be flawed. A systematic review of the literature to determine the following: (1) the relationship between CVP and blood volume, (2) the ability of CVP to predict fluid responsiveness, and (3) the ability of the change in CVP (DeltaCVP) to predict fluid responsiveness. MEDLINE, Embase, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Reported clinical trials that evaluated either the relationship between CVP and blood volume or reported the associated between CVP/DeltaCVP and the change in stroke volume/cardiac index following a fluid challenge. From 213 articles screened, 24 studies met our inclusion criteria and were included for data extraction. The studies included human adult subjects, healthy control subjects, and ICU and operating room patients. Data were abstracted on study design, study size, study setting, patient population, correlation coefficient between CVP and blood volume, correlation coefficient (or receive operator characteristic [ROC]) between CVP/DeltaCVP and change in stroke index/cardiac index, percentage of patients who responded to a fluid challenge, and baseline CVP of the fluid responders and nonresponders. Metaanalytic techniques were used to pool data. The 24 studies included 803 patients; 5 studies compared CVP with measured circulating blood volume, while 19 studies determined the relationship between CVP/DeltaCVP and change in cardiac performance following a fluid challenge. The pooled correlation coefficient between CVP and measured blood volume was 0.16 (95% confidence interval [CI], 0.03 to 0.28). Overall, 56+/-16% of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/cardiac index was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between DeltaCVP and change in stroke index/cardiac index was 0.11 (95% CI, 0.015 to 0.21). Baseline CVP was 8.7+/-2.32 mm Hg [mean+/-SD] in the responders as compared to 9.7+/-2.2 mm Hg in nonresponders (not significant). This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.

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Author and article information

Journal

Journal ID (nlm-ta): Crit Care

Journal ID (iso-abbrev): Crit Care

Title: Critical Care

Publisher: BioMed Central

ISSN (Print): 1364-8535

ISSN (Electronic): 1466-609X

Publication date (Print): 2012

Publication date (Electronic): 9 February 2012

Volume: 16

Issue: 1

Page: R23

Affiliations

[1 ]Department of Medicine, University of Southern California, 1520 San Pablo Street, Suite 4300, Los Angeles, CA, 90033 USA

[2 ]Department of Critical Care Medicine, University of Pittsburgh, Room 608, Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261 USA

[3 ]Department of Medicine, University College London Medical School, Rowland Hill Street, London NW3 2PF UK

[4 ]Department of Medicine, University of Toronto, 9th Floor Rm. 9N983, 200 Elizabeth Street, Toronto, ON M5G 2C4 Canada

[5 ]Department of Medicine, University of Washington, Box 356174, 1959 NE Pacific Street, Seattle, WA 98195, USA

[6 ]Department of Medicine, University of Alberta, 11-107 csb 8440 112 Street, Edmonton, Canada T6G 2G3, AB, Canada

[7 ]Department of Medicine, University of Alabama, ZRB 605, 1530 3rd Ave. S, Birmingham, AL 35294-0007 USA

[8 ]Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Alfred Centre, Commercial Rd, Prahran, Melbourne, Victoria 3181, Australia

[9 ]Department of Surgery, University of Southern California, 1510 San Pablo Street, Suite 200, Los Angeles, CA, 90033 USA

Article

Publisher ID: cc11188

DOI: 10.1186/cc11188

PMC ID: 3396267

PubMed ID: 22322077

SO-VID: 5e439e54-3e3a-4cdf-b2b4-4391680cb845

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 8 November 2011

Date revision received : 30 December 2011

Date accepted : 9 February 2012

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