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

Mitra K Nadim, John A Kellum, Andrew Davenport and 6 more

Critical Care · 2012 · Systematic review · CC BY

doi:10.1186/cc11188

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.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 25, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Hepatorenal syndrome (HRS) is a unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis. HRS is typically subdivided into two types: type-1 in which there is a rapid deterioration in kidney function with the serum creatinine (Scr) increasing by more than 100% from baseline to greater than 2.5 mg/dl within a two-week period, whereas type-2 HRS occurs in patients with refractory ascites with either a steady but moderate degree of functional renal failure (≥ 1.5 mg/dl) or a deterioration in kidney function that does not fulfill the criteria for HRS type-1. In patients with advanced cirrhosis, HRS is reported to occur in 18% within one year of diagnosis and up to 40% at five years. Untreated, median survival is two weeks for patients with type-1 HRS and four to six months in patients with type-2 HRS. However, many patients with lesser degrees of renal impairment in the setting of cirrhosis do not meet the precise definitions of HRS and, yet, have the same pathophysiological basis to their renal impairment and, therefore, could potentially benefit from therapies developed for HRS. A consensus conference under the auspices of the Acute Dialysis Quality Initiative (ADQI) was held in 2010. The purpose of this consensus conference was to review the literature on renal impairment in cirrhosis and to create the basis for a definition and classification system of all forms of renal impairment including HRS, from there to develop a broader understanding of its epidemiology, review current knowledge in the field of prevention and treatment, and develop the framework for a research agenda in relation to this condition.

ADQI process

ADQI is an ongoing process that seeks to produce evidence-based recommendations for the prevention and management of acute kidney injury (AKI) and on different issues concerning acute dialysis. It represents a non-profit association with an elected rotating board. ADQI conducts systematic reviews of the literature and provides expert-based statements and interpretation of current knowledge for use by clinicians according to professional judgment. The ADQI methods comprise (1) systemic search for evidence with review and evaluation of the available literature, (2) establishment of clinical and physiologic outcomes as well as measures to be used for comparison of different treatments, (3) description of the current practice and the rationale for use of current techniques, and (4) analysis of areas in which evidence is lacking and future research is required.

Prior to the conference, the organizing committee of ADQI VIII identified five topics relevant to the field of HRS (Table 1). We selected these topics with a set of key questions based on (1) prevalence of the associated clinical problem, (2) known variation in clinical practice, (3) availability of scientific evidence, (4) potential importance for clinical outcome, and (5) development of evidence-based medicine guidelines. For each topic, we outlined a preliminary set of key questions. We then assembled a diverse international panel representing multiple relevant disciplines (nephrology, hepatology, transplant surgery and critical care), from a variety of countries and scientific societies based on their expertise in AKI and HRS. Panelists were assigned to four to five person work groups, one of whom served as the group facilitator with each work group addressing one key topic.

ADQI activities were divided into a pre-conference, conference and post-conference phase. During the pre-conference phase, topics were selected, and the work groups were assembled and assigned to specific topics. Each group identified a list of key questions, conducted a systematic literature search and generated a bibliography of key studies. During this stage, the scope of the conference was also defined and some topics were excluded (Table 1). We then conducted a 2 1/2 -day conference. Our consensus process relied on evidence where available and, in the absence of evidence, consensus expert opinion where possible. The quality of the overall evidence and the strength of recommendations were graded using the Grading of Recommendations Assessment, Development and Evaluation system (Table 2). For interventions that have been studied using randomized trials we pooled the results of various trials using the Mantel-Haenszel method for calculating the weighted summary odds ratio under the fixed effects model. We also calculated the heterogeneity statistic and incorporated it to calculate the summary odds ratio under the random effects model. Both fixed and random effects models are reported.

During the conference, work groups assembled in breakout sessions, as well as in plenary sessions where their findings were presented, debated and refined. In each breakout session, the work groups refined the key questions, identified the supporting evidence, and generated practice recommendations and/or directions for future research as appropriate. A series of summary statements was then developed during the breakout sessions and presented to the entire group, revising each statement as needed until a final version was agreed upon. Directives for future research were achieved by asking the participants to identify deficiencies in the literature, determine if more evidence was necessary and if so, to articulate general research questions. When possible, pertinent study design issues were also considered. Final reports were summarized into a final conference document by a writing committee.

Systematic review of the literature

For each topic, the systematic review included the development of well specified research questions, literature searches, data extraction of primary studies and existing systematic reviews, tabulation of data, assessment of the quality of individual studies, and assessment of the overall quality of the literature and summary conclusions. Literature review was applied using key terms relevant to the topic and electronic reference libraries with the focus on human studies and limited to English language articles published between January 1960 and December 2009. Study eligibility was based on population, intervention, comparator, outcome, and study design relevant to each clinical question. Although nonrandomized studies were reviewed, the majority of the Work Group resources were devoted to review of randomized trials, as these were deemed to be most likely to provide data to support level 1 recommendations with very high- or high-quality (A or B) evidence. Exceptions were made for topics with sparse evidence. Each work group conducted literature searches related to their topic questions via MEDLINE, PubMed, data provided by the Scientific Registry of Transplant Recipients, Web of Science and the bibliographies of key reviews and of all articles that met the search criteria. Decisions to restrict the topics were made to focus the systematic reviews on those topics in which existing evidence was thought to be likely to provide support for the guideline.

Evaluation of studies

A three-phase approach was used to construct the evidence-based recommendations. The phases included a systematic literature review of studies in HRS and AKI in patients with cirrhosis, a comprehensive appraisal of prior studies, and convening an expert panel to synthesize this information and develop consensus based recommendations. The quality of the overall evidence and the strength of recommendations were graded using the Grading of Recommendations Assessment, Development and Evaluation system (Table 2). There were four categories for the quality of overall evidence, ranging from A to D. The strength of a recommendation was determined by the quality of the evidence and was graded Level 1, 2 or 'not graded". Recommendations were "Not Graded" if they were not based on systematic evidence and was used to provide guidance where the topic did not allow adequate application of evidence. Recommendation statements were developed from the systematic review, existing guidelines identified in the supplemental literature review, and expert opinion. Recommendations were developed by incorporating the best available evidence and expert opinion. Expert opinion was used when evidence in the literature did not exist to inform the decision. Recommendation statements were incorporated when they met one of two criteria: if there was strong literature-based evidence or if the expert panel voted that the recommendation was appropriate.

1. Serum creatinine measurements should be used to evaluate renal function in patients with advanced cirrhosis until more reliable methods of measuring renal function become generally available (1D)

Rationale: Serum creatinine (SCr) measurement remains the most practical and widely accepted method for estimating renal function in clinical practice in patients with cirrhosis and is the basis of existing definitions of AKI. The prognostic impact of renal function in liver disease is reflected by the inclusion of SCr in the Model for End-Stage Liver Disease (MELD) score, which is used to prioritize patients for liver transplantation. However, in cirrhosis, SCr is notoriously inaccurate in the diagnosis of renal dysfunction as it overestimates renal function due to decreased creatine production by the liver, protein calorie malnutrition, and muscle wasting. Furthermore, the measurement of SCr using the Jaffe method can be artificially lowered due to hyperbilirubinemia, or raised by cephalosporins leading to variability in MELD scores. Serum cystatin C has been suggested as a sensitive marker of renal function; however, recent studies have shown that like SCr, cystatin C is affected by age, gender, muscle mass and liver disease and overestimates renal function in patients with cirrhosis.

Glomerular filtration rate (GFR) is considered the best estimate of renal function although there is no universally accepted gold standard for its measurement. Clearance techniques using exogenous markers such as radiocontrast media, inulin or radioisotopes provide a more accurate measurement of GFR, but are labor intensive and expensive and appear to be susceptible to extra-renal clearance, overestimating GFR by as much as 20 mL/min/1.73 m2. For patients with liver disease, particularly those with advanced cirrhosis, none of the exogenous clearance markers have been rigorously studied. When properly performed, timed urinary collection of creatinine overcomes some of these limitations, but due to increased renal tubular creatinine secretion, creatinine clearance overestimates GFR measured by inulin clearance by a mean of 13 mL/min/1.73 m2.

2. GFR derived equations should be used cautiously for assessment of kidney function in cirrhosis since they tend to overestimate GFR (2D)

Rationale: The Cockcroft Gault and Modified Diet in Renal Disease (MDRD) equations are widely used to estimate GFR (eGFR) in the general population but consistently overestimate GFR in cirrhotic patients. The Cockcroft Gault equation is heavily influenced by weight as a reflection of lean body mass, which is not applicable to cirrhotic patients, in whom edema and ascites may account for a moderate and in some patients, even a substantial proportion of their weight. Several retrospective evaluations of SCr-based eGFR equations among liver transplant recipients suggest that the MDRD equations were best able to estimate GFR in comparison to radionucleotide GFR assessment; however, the precision of all GFR equations was poor. Other eGFR equations such as the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and cystatin C based eGFR, have been proposed; however, like the MDRD equations, they have not been validated in patients with liver disease. Therefore, we encourage very cautious use of these derived equations for the determination of GFR as they have not been validated in patients with liver disease.

Recommendations for future research:

• Formulate a specific equation for the calculation of GFR for patients with advanced cirrhosis by iohexol or inulin GFR determinations along with measurement of Scr and Cystatin C.

• Identify the role of ancillary renal testing such as diagnostic doppler ultrasound as epidemiological markers for patients with cirrhosis and renal dysfunction.

• Evaluate the value of renal injury biomarkers such as NGAL (neurtrophil gelatinase-associated lipocalin), IL-18 and KIM-1 (kidney-injury molecule) in the setting of AKI within the spectrum of hepatorenal disease.

1. Classify AKI in the setting of cirrhosis according to RIFLE criteria (Not Graded)

Rationale: In 1996, the International Ascites Club (IAC) proposed a definition and diagnostic criteria for HRS which was later revised in 2007 (Table 3). However, the rigid cut off value of SCr of ≥ 1.5 mg/dL has limited prompt management of patients with milder renal dysfunction. In 2004, the ADQI Workgroup developed a consensus definition and classification for AKI known as the RIFLE (Risk, Injury, Failure, Loss, End-Stage) criteria which stratified acute renal dysfunction into grades of increasing severity based on changes in SCr and/or urine output. Subsequently it was recognized that even smaller increases in SCr (absolute increase in SCr ≥ 0.3 mg/dL) are associated with adverse outcome. As a result, the criteria was modified in 2007 to broaden the definition of AKI (Table 4).

In critically ill patients with cirrhosis, AKI defined by RIFLE criteria has been shown to be a predictor of hospital survival. The final consensus of the workgroup was to apply the RIFLE criteria to define AKI in patients with cirrhosis irrespective of whether the cause of the acute deterioration in renal function was related to a functional or structural disorder (Table 5). This will certainly identify many patients with AKI with normal SCr but low GFR and allow us to extend treatment to patients at a lesser level of severity. In addition, the overall consensus was to also propose that the term hepatorenal disorders (HRD) be used to describe all patients with advanced cirrhosis and concurrent kidney dysfunction (Figure 1). HRD is thus defined as any form of kidney disease occurring in patients with cirrhosis, be it functional or structural in nature. Such a definition will allow cirrhotic patients with renal dysfunction to be properly classified, thereby allowing appropriate studies to be conducted to define their prognosis and to devise treatment options.

2. Classify CKD in the setting of cirrhosis according to Kidney Disease Outcomes Quality Initiatives (K/DOQI) (Not Graded)

Rationale: As mentioned above, estimation of GFR in cirrhosis is problematic; therefore, the application of the definition of CKD in cirrhosis is challenging. The Work Group accepted the definition of CKD, as set out by the practice guidelines from the K/DOQI Work Group, of an eGFR < 60 mL/min/1.73 m2 calculated using the MDRD-6 formula for more than three months for patients with cirrhosis (Table 5). Patients with type-2 HRS who meet these criteria should be considered as having CKD.

3. Acute on CKD in cirrhosis is defined as a rise in SCr ≥ 0.3 mg/dL in less than 48 hours or an increase in SCr ≥ 50% from baseline, or in a patient with cirrhosis whose baseline GFR has been < 60 ml/min calculated with the MDRD-6 formula for more than three months (Not Graded)

Rationale: It is important to recognize that AKI may also occur in patients with preexisting HRD. The group recognizes that acute on CKD does occur in cirrhosis and has defined it using the RIFLE criteria for AKI and K/DOQI guidelines for CKD (Table 5).

Recommendations for future research:

• Multicenter, prospective, epidemiologic (observational) studies to:

- Investigate the incidence, prevalence, basic demographics and outcomes of patients with HRD

- Validate new diagnostic criteria of AKI, CKD and acute on CKD for the cirrhotic population

- Determine whether the development of type-1 HRS in a patient with pre-existing type-2 HRS is the same as patients with pre-existing CKD

- Investigate the use of biomarkers to differentiate between type-1 HRS and other forms of AKI in patients with cirrhosis.

1. We suggest using hemodynamic monitoring, when possible, to help with the management of fluid balance in patients with HRS (2D)

Rationale: The key management strategy for patients admitted with cirrhosis is to avoid the development of HRS by preventing relative renal hypoperfusion, maintaining an effective circulating volume and renal perfusion pressure. Assessment of intravascular volume in patients with HRS, however, is challenging. Traditional methods based on clinical examination and static measurements of right atrial and pulmonary artery pressures are of questionable accuracy in predicting volume responsiveness and should be used with caution. Goal directed therapy with 20% albumin increased central blood volume and cardiac index, without subsequent changes in central venous pressure as any fluid bolus which initially expands the intravascular space, will subsequently expand the 'third space'. Functional hemodynamic monitoring, using continuous central venous pressures or indirect measurements of cardiac indices, should be used when possible to assess the short term response to a fluid volume bolus.

Although pulse pressure variation (PPV) derived from analysis of the arterial waveform and the stroke volume variation (SVV) derived from pulse contour analysis are predictive of fluid responsiveness in patients receiving volume-controlled mechanical ventilation, they are not as reliable in septic patients and those on pressure-support ventilation. Serial echocardiography can be used to assess changes in intravascular volume by measuring inferior vena caval diameter, right ventricular end-diastolic volume index, left ventricular end-diastolic area index, and the global end-diastolic volume index, but generally these are not as accurate as using PPV/SVV, are operator dependent and have not been evaluated in patients with cirrhosis.

2. We recommend that patients with type-1 HRS be optimally resuscitated with albumin (initially 1 g of albumin/kg for two days, up to a maximum of 100 g/day, followed by 20 to 40 g/day) in combination with a vasoconstrictor (1A), preferentially terlipressin (2C)

Rationale: The most effective method for treatment of type-1 HRS currently available is the administration of systemic vasoconstrictor drugs (Table 6) in order to reduce the marked vasodilatation in the splanchnic and systemic circulations thereby improving the associated impaired circulatory function. Although randomized controlled trials and meta-analysis of the combination of terlipressin and albumin have been shown to reverse HRS type 1 and improve renal function in patients with type-1 HRS (Figure 2), data regarding survival benefit has been limited although it may allow survival to transplantation (Figure 3). Therapy should be discontinued after four days in non-responders and only continued thereafter in partial responders (SCr improves, but does not decrease to < 1.5 mg/dL). As terlipressin can cause organ ischemia, it is contraindicated in patients with ischemic heart disease, peripheral vascular disease and/or cerebrovascular disease and all patients should be monitored closely for cardiac arrhythmias or signs of splanchnic or digital ischemia. If terlipressin is unavailable, alternative vasoconstrictors such as norepinephrine, vasopressin or a combination of octreotide and midodrine, together with albumin should be considered. Currently there are no randomized trials showing superiority of terlipressin in comparison to other vasoconstrictors.

Recommendations for future research:

• Comparative randomized controlled trials of vasoconstrictors are required to determine the merits of vasopressin analogues, specifically terlipressin, against alpha-adrenergic agents in patients with type-1 HRS.

• Randomized controlled trials of vasoconstrictors in patients with type-2 HRS.

1. We recommend withholding renal replacement therapy (RRT) in patients with decompensation of cirrhosis who are not candidates for liver transplantation (1D)

Rationale: RRT improves short-term survival in severe AKI and can be helpful in bridging patients to transplant or treating patients who have acute but reversible decompensation. Although there is a preference for continuous renal replacement therapy (CRRT) over intermittent hemodialysis in hemodynamically unstable patients, analysis of the currently published studies does not allow evidence-based guidelines for the selection of RRT modality for the treatment of AKI in the setting of HRS. CRRT use may be advantageous in the management of HRS patients with AKI who are hemodynamically unstable or those patients at risk of elevated intracranial pressure such as patients with acute fulminant liver failure or acute on chronic liver failure. However, prognosis in type-1 HRS is very poor and RRT should be avoided in these patients unless there is either an acute reversible component or a plan for liver transplantation.

2. We suggest that artificial liver support therapies for HRS be limited to research protocols (2D)

Rationale: Extracorporeal support systems in liver disease can be divided into two broad categories: non-cell and cell-based systems (Table 7). Non-cell based systems do not incorporate tissue and provide only detoxification functions using membranes and adsorbents. These newer developing therapies are expensive and have not as yet demonstrated a survival benefit in patients with type-1 HRS despite improvements in neurological function and coagulation indices. Molecular Adsorbent Recirculating System (MARS) is now commercially available in the US and Europe. Although MARS therapy has not demonstrated a definite survival benefit in patients with liver disease, it has been shown to improve hepatic encephalopathy (Figures 4, 5). Cell-based systems aim to provide the excretory, synthetic, and metabolic functions of the liver using living liver cells. In addition to detoxification, cell-based systems can also provide some synthetic and regulatory functions; however, they have mainly been tested in single-center phase I and II trials, and none have yet received US Food and Drug Administration (FDA) approval.

Recommendations for future research:

• Further observational studies and ultimately randomized controlled trials directed to the identification of the appropriate indications, timing of intervention, and cost effectiveness of supportive detoxification therapies. Consequently, the most appropriate outcome for studies would be short-term survival as a bridge to transplantation.

1. We recommend use of a transjugular intrahepatic portosystemic shunt (TIPS) as a treatment option for patients with type-2 HRS with refractory ascites who require large-volume paracentesis (1C)

Rationale: Very few studies have assessed the role of TIPS in patients with HRS (Table 8). In patients with type-2 HRS, TIPS has been shown to improve refractory ascites and improve renal function without improvement in survival. However, new hepatic encephalopathy, deterioration of previous hepatic encephalopathy or mild and transient deterioration of liver function tests has been reported following TIPS. In patients with type-1 HRS, TIPS may improve renal function and survival; however, there is insufficient data to support the use of TIPS as a first-line treatment of patients with type-1 HRS. TIPS is not recommended in patients with severe liver failure defined as serum bilirubin > 5 mg/dl, INR > 2 or Child-Pugh score > 11, hepatic encephalopathy or severe cardiopulmonary diseases.

2. We suggest liver transplantation alone for candidates with type-1 HRS for less than four weeks and simultaneous liver-kidney (SLK) for those at risk for non-recovery of renal function (2D)

Rationale: As the waiting time for liver transplantation has increased, the incidence of pre-transplant renal dysfunction and RRT has also increased. In patients with renal dysfunction at the time of liver transplantation (LT), it is important to know whether renal function will improve, stabilize or continue to progress following transplantation. However, the level and duration of renal dysfunction, including RRT, beyond which renal recovery is not possible following LT alone is unknown. Several investigators have studied the impact of pre-transplant AKI on post transplant outcomes; however, the small study sample size, retrospective design, reporting bias, and variation in definitions used to define renal dysfunction hinders comparison between these studies.

Currently there are no standard criteria for the evaluation, selection and/or allocation of a kidney at the time of LT. Despite an increase in the rate of SLK transplantation immediately following the implementation of the MELD allocation system in March 2002 (Figure 6), recent Organ Procurement and Transplantation Network (OPTN) data suggest a decrease since 2007 which may be due to consensus guidelines published at that time. Based on the published consensus guidelines, the OPTN Liver and Intestine Committee and Kidney Committee recently developed proposed listing criteria for SLK candidate selection and allocation (Policy 3.5.10) (Table 9).

The duration of pre-liver transplant kidney dysfunction or dialysis that is amenable to recovery is not known. Retrospective studies from single centers have shown the importance of the duration of > 12 weeks of SCr ≥ 1.5 mg/dL and dialysis ≤ 4 weeks pre-transplant on post transplant renal outcomes. However, the renal outcome of patients dialyzed for > 4 weeks is unknown as many of these patients frequently undergo SLK. Timing of dialysis is related to numerous factors and is a complex process. Since a threshold of dialysis duration that is sufficiently predictive of renal recovery has not been established, and also because initiation of dialysis is physician/center dependent, dialysis duration as a criterion for SLK should be used with caution in patients who do not have end-stage renal disease. The decision for SLK versus LT alone should be undertaken with consideration of duration of HRS, AKI and CKD and risk factors for progression of CKD present at the time of liver transplant such as hypertension, diabetes and obesity. Currently there are several pitfalls with the SLK guidelines such as definition of AKI, GFR determination, timing of initiation of dialysis and duration of dialysis. To that end, the ADQI group unanimously agreed that using the existing literature is not sufficient to allow guidelines or criteria to be set.

Recommendations for future research:

• Multicenter, prospective, observational studies in patients undergoing SLK to determine:

- The predictive value of RIFLE classifications pre-transplant on post liver transplant outcomes

- Which RIFLE class and for what duration of AKI pre-transplant is associated with rates of renal recovery that warrant SLK

- What is the recovery rate of native kidney function in patients with pre-transplant type-1 or 2 HRS

• Epidemiologic studies that document long-term patient and renal outcomes and the prognostic factors for these outcomes in patients with HRS who receive LT alone, who recover residual renal function, remain on dialysis and those subsequently receiving renal transplantation.

Conclusions

Since first defined in 1996 by the IAC, there has been substantial progress towards understanding the pathogenesis and natural history of HRS. However, there remains a significant deficiency in our knowledge regarding its management. The IAC has set out clear diagnostic criteria for both acute and chronic forms of HRS, but has not delineated guidelines for the diagnosis of other forms of renal impairment in cirrhosis, be they acute or chronic. Well-accepted definitions and staging systems for CKD and AKI exist, but have not been consistently applied to patients with advanced liver disease. Indeed, it must be understood that although our recommendations are based, to the best extent possible, on data, there are insufficient data to guide many important decisions. In addition, although our Work Group included a wide range of specialists from around the world, we do recognize that there exists regional heterogeneity in practice. As a result, our findings should be considered a 'first step' in the process of standardization of the definition of AKI in patients with cirrhosis. Once agreed, these new diagnostic criteria of AKI for cirrhosis will need to be validated and the threshold for the diagnosis of type-1 HRS may need to be revised to a lower target value to allow patients with a lesser degree of SCr rise to receive prompt appropriate treatment. In addition, criteria for SLK may need to be revisited in lieu of the new classification and to determine whether the new classification and definition will improve patient outcomes. One clear conclusion of this ADQI meeting is that multicenter, prospective, long-term outcome studies in patients with advanced cirrhosis and HRS are urgently needed.

Key messages

• The ADQI Work Group recommends incorporation of the modified RIFLE criteria to define AKI in patients with cirrhosis irrespective of whether the cause of the acute deterioration in renal function is related to a functional or structural discorder.

• Regarding the current state of combined liver-kidney transplantation in patients with cirrhosis and kidney disease, including HRS, the ADQI group unanimously agreed that using the existing literature is not sufficient to allow guidelines or criteria to be set.

• Multicenter prospective, long-term outcome studies in patients with advanced cirrhosis and HRS are urgently needed.

Abbreviations

ADQI: Acute Dialysis Quality Initiative; AKI: acute kidney injury; CKD: chronic kidney disease; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; CRRT: continuous renal replacement therapy; eGFR: estimated glomerular filtration rate; FDA: Food and Drug Administration; GFR: glomerular filtration rate; HRD: hepatorenal disorders; HRS: hepatorenal syndrome; IAC: International Ascites Club; IL: interleukin; KIM-1: kidney-injury molecule 1; K/DOQI: Kidney Disease Outcomes Quality Initiatives; LT: liver transplantation; MARS: molecular adsorbent recirculating system; MDRD: Modified Diet in Renal Disease; MELD: Model for End-Stage Liver Disease; NGAL: neurtrophil gelatinase-associated lipocalin; OPTN: Organ Procurement and Transplantation Network; PPV: pulse pressure variation; RIFLE: risk: injury: failure: loss: end-stage; RRT: renal replacement therapy; Scr: serum creatinine; SLK: simultaneous liver-kidney; SVV: stroke volume variation; TIPS: transjugular intrahepatic portosystemic shunt.

Competing interests

ADQI is supported by a group of sponsors and no funding is accepted for the development of specific guidelines and every effort is made by to avoid any actual or perceived conflicts of interest that may arise as a result of an outside relationship of a member of the ADQI Work Group. Prior to the meeting, all members of the Work Group are required to complete, sign and submit a disclosure and attestation form showing all their relationships that might be actual or perceived conflicts of interest. None of the companies that provided financial support for this meeting were involved in any way in the organization of the meeting, the decision regarding invited faculty, the design and contents of the meeting, the collection, management, analysis, and interpretation of the data, and preparation, review, or approval of the manuscript. MKN has served as an advisor for Ikaria and has also served as a speaker for Gambro. JAK has served as a consultant and has received grant support from Gambro and Baxter. AT, JC and NG have served as speakers for Gambro. CD has served as an advisor for Ikaria. The other 13 members of the Work Group reported no relevant financial relationships.

Authors' contributions

MKN, JAK and YSG were the main organizers of this meeting and helped to draft the manuscript. AD, CD, NP, RB, FW and AT were the facilitators for each Work Group and participated in drafting the sections that were related to their Work Group. All authors read and approved the final manuscript.

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  18. 18.

    Cholongitas E Marelli L Kerry A Senzolo M Goodier DW Nair D Thomas M Patch D Burroughs AK Different methods of creatinine measurement significantly affect MELD scoresLiver Transpl2007 13523529

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  21. 21.

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  30. 30.

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  41. 41.
    Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group · 2004
    No notice
  42. 42.

    Lassnigg A Schmidlin D Mouhieddine M Bachmann LM Druml W Bauer P Hiesmayr M Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort studyJ Am Soc Nephrol2004 1515971605

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  43. 43.
    Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury · 2007
    No notice
  44. 44.

    Jenq CC Tsai MH Tian YC Lin CY Yang C Liu NJ Lien JM Chen YC Fang JT Chen PC Yang CW RIFLE classification can predict short-term prognosis in critically ill cirrhotic patientsIntensive Care Med2007 3319211930

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    Wong F Nadim MK Kellum JA Salerno F Bellomo R Gerbes A Angeli P Moreau R Davenport A Jalan R Ronco C Genyk Y Arroyo V Working Party proposal for a revised classification system of renal dysfunction in patients with cirrhosisGut2011 60702709

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    Marik PE Baram M Vahid B Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven maresChest2008 134172178

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  53. 53.

    Perner A Faber T Stroke volume variation does not predict fluid responsiveness in patients with septic shock on pressure support ventilationActa Anaesthesiol Scand2006 5010681073

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  54. 54.

    Umgelter A Reindl W Wagner KS Franzen M Stock K Schmid RM Huber W Effects of plasma expansion with albumin and paracentesis on haemodynamics and kidney function in critically ill cirrhotic patients with tense ascites and hepatorenal syndrome: a prospective uncontrolled trialCrit Care2008 12R4

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    Umgelter A Reindl W Franzen M Lenhardt C Huber W Schmid RM Renal resistive index and renal function before and after paracentesis in patients with hepatorenal syndrome and tense ascitesIntensive Care Med2009 35152156

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    Kiser TH Maclaren R Fish DN Treatment of hepatorenal syndromePharmacotherapy2009 2911961211

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    Moller S Bendtsen F Henriksen JH Pathophysiological basis of pharmacotherapy in the hepatorenal syndromeScand J Gastroenterol2005 40491500

    Not in our library10.1080/00365520510012064

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    Hadengue A Gadano A Moreau R Giostra E Durand F Valla D Erlinger S Lebrec D Beneficial effects of the 2-day administration of terlipressin in patients with cirrhosis and hepatorenal syndromeJ Hepatol1998 29565570

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    Uriz J Gines P Cardenas A Sort P Jimenez W Salmeron JM Bataller R Mas A Navasa M Arroyo V Rodes J Terlipressin plus albumin infusion: an effective and safe therapy of hepatorenal syndromeJ Hepatol2000 334348

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    Solanki P Chawla A Garg R Gupta R Jain M Sarin SK Beneficial effects of terlipressin in hepatorenal syndrome: a prospective, randomized placebo-controlled clinical trialJ Gastroenterol Hepatol2003 18152156

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    Testro AG Wongseelashote S Angus PW Gow PJ Long-term outcome of patients treated with terlipressin for types 1 and 2 hepatorenal syndromeJ Gastroenterol Hepatol2008 2315351540

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    Nazar A Pereira GH Guevara M Martin-Llahi M Pepin MN Marinelli M Sola E Baccaro ME Terra C Arroyo V Gines P Predictors of response to therapy with terlipressin and albumin in patients with cirrhosis and type 1 hepatorenal syndromeHepatology2010 51219226

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    Neri S Pulvirenti D Malaguarnera M Cosimo BM Bertino G Ignaccolo L Siringo S Castellino P Terlipressin and albumin in patients with cirrhosis and type I hepatorenal syndromeDig Dis Sci2008 53830835

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    Ortega R Gines P Uriz J Cardenas A Calahorra B De Las Heras D Guevara M Bataller R Jimenez W Arroyo V Rodes J Terlipressin therapy with and without albumin for patients with hepatorenal syndrome: results of a prospective, nonrandomized studyHepatology2002 36941948

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    Sagi SV Mittal S Kasturi KS Sood GK Terlipressin therapy for reversal of type 1 hepatorenal syndrome: a meta-analysis of randomized controlled trialsJ Gastroenterol Hepatol25880885

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    Sanyal AJ Boyer T Garcia-Tsao G Regenstein F Rossaro L Appenrodt B Blei A Gulberg V Sigal S Teuber P A randomized, prospective, double-blind, placebo-controlled trial of terlipressin for type 1 hepatorenal syndromeGastroenterology2008 13413601368

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    Sharma P Kumar A Shrama BC Sarin SK An open label, pilot, randomized controlled trial of noradrenaline versus terlipressin in the treatment of type 1 hepatorenal syndrome and predictors of responseAm J Gastroenterol2008 10316891697

    Not in our library10.1111/j.1572-0241.2008.01828.x

  70. 70.

    Moreau R Durand F Poynard T Duhamel C Cervoni JP Ichai P Abergel A Halimi C Pauwels M Bronowicki JP Giostra E Fleurot C Gurnot D Nouel O Renard P Rivoal M Blanc P Coumaros D Ducloux S Levy S Pariente A Perarnau JM Roche J Scribe-Outtas M Valla D Bernard B Samuel D Butel J Hadengue A Platek A Terlipressin in patients with cirrhosis and type 1 hepatorenal syndrome: a retrospective multicenter studyGastroenterology2002 122923930

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    Martin-Llahi M Pepin MN Guevara M Diaz F Torre A Monescillo A Soriano G Terra C Fabrega E Arroyo V Rodes J Gines P Terlipressin and albumin vs albumin in patients with cirrhosis and hepatorenal syndrome: a randomized studyGastroenterology2008 13413521359

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    Krag A Moller S Henriksen JH Holstein-Rathlou NH Larsen FS Bendtsen F Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndromeHepatology2007 4618631871

    Not in our library10.1002/hep.21901

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    Halimi C Bonnard P Bernard B Mathurin P Mofredj A di Martino V Demontis R Henry-Biabaud E Fievet P Opolon P Poynard T Cadranel JF Effect of terlipressin (Glypressin) on hepatorenal syndrome in cirrhotic patients: results of a multicentre pilot studyEur J Gastroenterol Hepatol2002 14153158

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    Gerbes AL Huber E Gulberg V Terlipressin for hepatorenal syndrome: continuous infusion as an alternative to i.v. bolus administrationGastroenterology2009 1371179

    Not in our library10.1053/j.gastro.2009.03.064

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    Colle I Durand F Pessione F Rassiat E Bernuau J Barriere E Lebrec D Valla DC Moreau R Clinical course, predictive factors and prognosis in patients with cirrhosis and type 1 hepatorenal syndrome treated with Terlipressin: a retrospective analysisJ Gastroenterol Hepatol2002 17882888

    Not in our library10.1046/j.1440-1746.2002.02816.x

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    Danalioglu A Cakaloglu Y Karaca C Aksoy N Akyuz F Ozdil S Demir K Besisik F Boztas G Mungan Z Kaymakoglu S Okten A Terlipressin and albumin combination treatment in hepatorenal syndromeHepatogastroenterology2003 50303305

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    Alessandria C Ottobrelli A Debernardi-Venon W Todros L Cerenzia MT Martini S Balzola F Morgando A Rizzetto M Marzano A Noradrenalin vs terlipressin in patients with hepatorenal syndrome: a prospective, randomized, unblinded, pilot studyJ Hepatol2007 47499505

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    Fabrizi F Dixit V Messa P Martin P Terlipressin for hepatorenal syndrome: A meta-analysis of randomized trialsInt J Artif Organs2009 32133140

    Not in our library

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    Gluud LL Christensen K Christensen E Krag A Systematic review of randomized trials on vasoconstrictor drugs for hepatorenal syndromeHepatology2010 51576584

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    Duvoux C Zanditenas D Hezode C Chauvat A Monin JL Roudot-Thoraval F Mallat A Dhumeaux D Effects of noradrenalin and albumin in patients with type I hepatorenal syndrome: a pilot studyHepatology2002 36374380

    Not in our library10.1053/jhep.2002.34343

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    Kiser TH Fish DN Obritsch MD Jung R MacLaren R Parikh CR Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective studyNephrol Dial Transplant2005 2018131820

    Not in our library10.1093/ndt/gfh930

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    Skagen C Einstein M Lucey MR Said A Combination treatment with octreotide, midodrine, and albumin improves survival in patients with type 1 and type 2 hepatorenal syndromeJ Clin Gastroenterol2009 43680685

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    Tandon P Tsuyuki RT Mitchell L Hoskinson M Ma MM Wong WW Mason AL Gutfreund K Bain VG The effect of 1 month of therapy with midodrine, octreotide-LAR and albumin in refractory ascites: a pilot studyLiver Int2009 29169174

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    Wong F Pantea L Sniderman K Midodrine, octreotide, albumin, and TIPS in selected patients with cirrhosis and type 1 hepatorenal syndromeHepatology2004 405564

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    Esrailian E Pantangco ER Kyulo NL Hu KQ Runyon BA Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndromeDig Dis Sci2007 52742748

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    Alessandria C Debernardi-Venon W Carello M Ceretto S Rizzetto M Marzano A Midodrine in the prevention of hepatorenal syndrome type 2 recurrence: a case-control studyDig Liver Dis2009 41298302

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    Angeli P Volpin R Gerunda G Craighero R Roner P Merenda R Amodio P Sticca A Caregaro L Maffei-Faccioli A Gatta A Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotideHepatology1999 2916901697

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    Witzke O Baumann M Patschan D Patschan S Mitchell A Treichel U Gerken G Philipp T Kribben A Which patients benefit from hemodialysis therapy in hepatorenal syndrome?J Gastroenterol Hepatol2004 1913691373

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    Davenport A Bouman C Kirpalani A Skippen P Tolwani A Mehta RL Palevsky PM Delivery of renal replacement therapy in acute kidney injury: what are the key issues?Clin J Am Soc Nephrol2008 3869875

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    Bellomo R Cass A Cole L Finfer S Gallagher M Lo S McArthur C McGuinness S Myburgh J Norton R Scheinkestel C Su S Intensity of continuous renal-replacement therapy in critically ill patientsN Engl J Med2009 36116271638

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    Kellum JA Angus DC Johnson JP Leblanc M Griffin M Ramakrishnan N Linde-Zwirble WT Continuous versus intermittent renal replacement therapy: a meta-analysisIntensive Care Med2002 282937

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    Tonelli M Manns B Feller-Kopman D Acute renal failure in the intensive care unit: a systematic review of the impact of dialytic modality on mortality and renal recoveryAm J Kidney Dis2002 40875885

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    Palevsky PM Zhang JH O'Connor TZ Chertow GM Crowley ST Choudhury D Finkel K Kellum JA Paganini E Schein RM Smith MW Swanson KM Thompson BT Vijayan A Watnick S Star RA Peduzzi P Intensity of renal support in critically ill patients with acute kidney injuryN Engl J Med2008 359720

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    Davenport A Will EJ Davison AM Swindells S Cohen AT Miloszewski KJ Losowsky MS Changes in intracranial pressure during haemofiltration in oliguric patients with grade IV hepatic encephalopathyNephron1989 53142146

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    Chang TM Haemoperfusions over microencapsulated adsorbent in a patient with hepatic comaLancet1972 213711372

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    Bihari D Hughes RD Gimson AE Langley PG Ede RJ Eder G Williams R Effects of serial resin hemoperfusion in fulminant hepatic failureInt J Artif Organs1983 6299302

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    Gimson AE Braude S Mellon PJ Canalese J Williams R Earlier charcoal haemoperfusion in fulminant hepatic failureLancet1982 2681683

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  100. 100.

    O'Grady JG Gimson AE O'Brien CJ Pucknell A Hughes RD Williams R Controlled trials of charcoal hemoperfusion and prognostic factors in fulminant hepatic failureGastroenterology1988 9411861192

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    Gazzard BG Weston MJ Murray-Lyon IM Flax H Record CO Williams R Portmann B Langley PG Dunlop EH Mellon PJ Ward MD Charcoal haemoperfusion in the treatment of fulminant hepatic failureLancet1974 113011307

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    Ellis AJ Hughes RD Nicholl D Langley PG Wendon JA O'Grady JG Williams R Temporary extracorporeal liver support for severe acute alcoholic hepatitis using the BioLogic-DTInt J Artif Organs1999 222734

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    Hughes RD Pucknell A Routley D Langley PG Wendon JA Williams R Evaluation of the BioLogic-DT sorbent-suspension dialyser in patients with fulminant hepatic failureInt J Artif Organs1994 17657662

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    Ash SR Blake DE Carr DJ Carter C Howard T Makowka L Clinical effects of a sorbent suspension dialysis system in treatment of hepatic coma (the BioLogic-DT)Int J Artif Organs1992 15151161

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    Wilkinson AH Ash SR Nissenson AR Hemodiabsorption in treatment of hepatic failureJ Transpl Coord1998 84350

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    Lepore MJ Martel AJ Plasmapheresis with plasma exchange in hepatic coma. Methods and results in five patients with acute fulminant hepatic necrosisAnn Intern Med1970 72165174

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    Lepore MJ Stutman LJ Bonanno CA Conklin EF Robilotti JG Jr McKenna PJ Plasmapheresis with plasma exchange in hepatic coma. II. Fulminant viral hepatitis as a systemic diseaseArch Intern Med1972 129900907

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    Yoshiba M Sekiyama K Iwamura Y Sugata F Development of reliable artificial liver support (ALS)--plasma exchange in combination with hemodiafiltration using high-performance membranesDig Dis Sci1993 38469476

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    Kondrup J Almdal T Vilstrup H Tygstrup N High volume plasma exchange in fulminant hepatic failureInt J Artif Organs1992 15669676

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    Clemmesen JO Gerbes AL Gulberg V Hansen BA Larsen FS Skak C Tygstrup N Ott P Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high-volume plasmapheresisHepatology1999 29347355

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    Morimoto T Matsushima M Sowa N Ide K Sawanishi K Plasma adsorption using bilirubin-adsorbent materials as a treatment for patients with hepatic failureArtif Organs1989 13447452

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    Ott R Rupprecht H Born G Muller V Reck T Hohenberger W Kockerling F Plasma separation and bilirubin adsorption after complicated liver transplantation: a therapeutic approach to excessive hyperbilirubinemiaTransplantation1998 65434437

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    Tabei K Akai Y Takeda S Homma S Kusano E Asano Y Application of plasma perfusion in hepatic failureBiomater Artif Cells Immobilization Biotechnol1991 19193201

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    Rozga J Umehara Y Trofimenko A Sadahiro T Demetriou AA A novel plasma filtration therapy for hepatic failure: preclinical studiesTher Apher Dial2006 10138144

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    Li LJ Yang Q Huang JR Xu XW Chen YM Fu SZ Effect of artificial liver support system on patients with severe viral hepatitis: a study of four hundred casesWorld J Gastroenterol2004 1029842988

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    Geiger H Klepper J Lux P Heidland A Biochemical assessment and clinical evaluation of a bilirubin adsorbent column (BR-350) in critically ill patients with intractable jaundiceInt J Artif Organs1992 153539

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    Senf R Klingel R Kurz S Tullius S Sauer I Frei U Schindler R Bilirubin-adsorption in 23 critically ill patients with liver failureInt J Artif Organs2004 27717722

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    Karvellas CJ Bagshaw SM McDermid RC Stollery DE Bain VG Gibney RT A case-control study of single-pass albumin dialysis for acetaminophen-induced acute liver failureBlood Purif2009 28151158

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    Rahman E Al Suwaida AK Askar A Single pass albumin dialysis in hepatorenal syndromeSaudi J Kidney Dis Transpl2008 19479484

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    Chawla LS Georgescu F Abell B Seneff MG Kimmel PL Modification of continuous venovenous hemodiafiltration with single-pass albumin dialysate allows for removal of serum bilirubinAm J Kidney Dis2005 45e5156

    Not in our library10.1053/j.ajkd.2004.11.023

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    Boonsrirat U Tiranathanagul K Srisawat N Susantitaphong P Komolmit P Praditpornsilpa K Tungsanga K Eiam-Ong S Effective bilirubin reduction by single-pass albumin dialysis in liver failureArtif Organs2009 33648653

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    Vienken J Christmann H How can liver toxins be removed? Filtration and adsorption with the Prometheus systemTher Apher Dial2006 10125131

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  123. 123.

    Rifai K Ernst T Kretschmer U Hafer C Haller H Manns MP Fliser D The Prometheus device for extracorporeal support of combined liver and renal failureBlood Purif2005 23298302

    Not in our library10.1159/000086552

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    Rifai K Ernst T Kretschmer U Bahr MJ Schneider A Hafer C Haller H Manns MP Fliser D Prometheus--a new extracorporeal system for the treatment of liver failureJ Hepatol2003 39984990

    Not in our library10.1016/s0168-8278(03)00468-9

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    Khuroo MS Farahat KL Molecular adsorbent recirculating system for acute and acute-on-chronic liver failure: a meta-analysisLiver Transpl2004 1010991106

    Not in our library10.1002/lt.20139

  126. 126.

    Mitzner SR Stange J Klammt S Risler T Erley CM Bader BD Berger ED Lauchart W Peszynski P Freytag J Hickstein H Loock J Lohr JM Liebe S Emmrich J Korten G Schmidt R Improvement of hepatorenal syndrome with extracorporeal albumin dialysis MARS: results of a prospective, randomized, controlled clinical trialLiver Transpl2000 6277286

    Not in our library10.1053/lv.2000.6355

  127. 127.

    Wong F Raina N Richardson R Molecular adsorbent recirculating system is ineffective in the management of type 1 hepatorenal syndrome in patients with cirrhosis with ascites who have failed vasoconstrictor treatmentGut2010 59381386

    Not in our library10.1136/gut.2008.174615

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    Hassanein TI Tofteng F Brown RS Jr McGuire B Lynch P Mehta R Larsen FS Gornbein J Stange J Blei AT Randomized controlled study of extracorporeal albumin dialysis for hepatic encephalopathy in advanced cirrhosisHepatology2007 4618531862

    Not in our library10.1002/hep.21930

  129. 129.

    Camus C Lavoue S Gacouin A Compagnon P Boudjema K Jacquelinet C Thomas R Le Tulzo Y Liver transplantation avoided in patients with fulminant hepatic failure who received albumin dialysis with the molecular adsorbent recirculating system while on the waiting list: impact of the duration of therapyTher Apher Dial2009 13549555

    Not in our library10.1111/j.1744-9987.2009.00708.x

  130. 130.

    Heemann U Treichel U Loock J Philipp T Gerken G Malago M Klammt S Loehr M Liebe S Mitzner S Schmidt R Stange J Albumin dialysis in cirrhosis with superimposed acute liver injury: a prospective, controlled studyHepatology2002 36949958

    Not in our library10.1053/jhep.2002.36130

  131. 131.

    Sen S Davies NA Mookerjee RP Cheshire LM Hodges SJ Williams R Jalan R Pathophysiological effects of albumin dialysis in acute-on-chronic liver failure: a randomized controlled studyLiver Transpl2004 1011091119

    Not in our library10.1002/lt.20236

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    Sauer IM Kardassis D Zeillinger K Pascher A Gruenwald A Pless G Irgang M Kraemer M Puhl G Frank J Muller AR Steinmuller T Denner J Neuhaus P Gerlack JC Clinical extracorporeal hybrid liver support--phase I study with primary porcine liver cellsXenotransplantation2003 10460469

    Not in our library10.1034/j.1399-3089.2003.00062.x

  133. 133.

    Hui T Rozga J Demetriou AA Bioartificial liver supportJ Hepatobiliary Pancreat Surg2001 8115

    Not in our library10.1007/s005340170045

  134. 134.

    Sauer IM Zeilinger K Obermayer N Pless G Grunwald A Pascher A Mieder T Roth S Goetz M Kardassis D Mas A Neuhaus P Gerlach JC Primary human liver cells as source for modular extracorporeal liver support--a preliminary reportInt J Artif Organs2002 2510011005

    Not in our library10.1177/039139880202501015

  135. 135.

    Brensing KA Textor J Strunk H Klehr HU Schild H Sauerbruch T Transjugular intrahepatic portosystemic stent-shunt for hepatorenal syndromeLancet1997 349697698

    Not in our library10.1016/s0140-6736(97)24010-9

  136. 136.

    Guevara M Gines P Bandi JC Gilabert R Sort P Jimenez W Garcia-Pagan JC Bosch J Arroyo V Rodes J Transjugular intrahepatic portosystemic shunt in hepatorenal syndrome: effects on renal function and vasoactive systemsHepatology1998 28416422

    Not in our library10.1002/hep.510280219

  137. 137.

    Brensing KA Textor J Perz J Schiedermaier P Raab P Strunk H Klehr HU Kramer HJ Spengler U Schild H Sauerbruch T Long term outcome after transjugular intrahepatic portosystemic stent-shunt in non-transplant cirrhotics with hepatorenal syndrome: a phase II studyGut2000 47288295

    Not in our library10.1136/gut.47.2.288

  138. 138.

    Testino G Ferro C Sumberaz A Messa P Morelli N Guadagni B Ardizzone G Valente U Type-2 hepatorenal syndrome and refractory ascites: role of transjugular intrahepatic portosystemic stent-shunt in eighteen patients with advanced cirrhosis awaiting orthotopic liver transplantationHepatogastroenterology2003 5017531755

    Not in our library

  139. 139.

    Cabezuelo JB Ramirez P Rios A Acosta F Torres D Sansano T Pons JA Bru M Montoya M Bueno FS Robles R Parrilla P Risk factors of acute renal failure after liver transplantationKidney Int2006 6910731080

    Not in our library10.1038/sj.ki.5000216

  140. 140.

    Campbell MS Kotlyar DS Brensinger CM Lewis JD Shetty K Bloom RD Markmann JF Olthoff KM Shaked A Reddy KR Renal function after orthotopic liver transplantation is predicted by duration of pretransplantation creatinine elevationLiver Transpl2005 1110481055

    Not in our library10.1002/lt.20445

  141. 141.

    Kurstein P Gluud LL Willemann M Olsen KR Kjellberg J Sogaard J Gluud C Agreement between reported use of interventions for liver diseases and research evidence in Cochrane systematic reviewsJ Hepatol2005 43984989

    Not in our library10.1016/j.jhep.2005.06.017

  142. 142.

    Pawarode A Fine DM Thuluvath PJ Independent risk factors and natural history of renal dysfunction in liver transplant recipientsLiver Transpl2003 9741747

    Not in our library10.1053/jlts.2003.50113

  143. 143.

    Bahirwani R Campbell MS Siropaides T Markmann J Olthoff K Shaked A Bloom RD Reddy KR Transplantation: impact of pretransplant renal insufficiencyLiver Transpl2008 14665671

    Not in our library10.1002/lt.21367

  144. 144.

    Ruiz R Kunitake H Wilkinson AH Danovitch GM Farmer DG Ghobrial RM Yersiz H Hiatt JR Busuttil RW Long-term analysis of combined liver and kidney transplantation at a single centerArch Surg2006 141735741

    Not in our library10.1001/archsurg.141.8.735

  145. 145.

    Ruiz R Barri YM Jennings LW Chinnakotla S Goldstein RM Levy MF McKenna GJ Randall HB Sanchez EQ Klintmalm GB Hepatorenal syndrome: a proposal for kidney after liver transplantation (KALT)Liver Transpl2007 13838843

    Not in our library10.1002/lt.21149

  146. 146.

    Davis CL Feng S Sung R Wong F Goodrich NP Melton LB Reddy KR Guidinger MK Wilkinson A Lake J Simultaneous liver-kidney transplantation: evaluation to decision makingAm J Transplant2007 717021709

    Not in our library10.1111/j.1600-6143.2007.01856.x

  147. 147.

    Eason JD Gonwa TA Davis CL Sung RS Gerber D Bloom RD Proceedings of Consensus Conference on Simultaneous Liver Kidney Transplantation (SLK)Am J Transplant2008 822432251

    Not in our library10.1111/j.1600-6143.2008.02416.x

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