Acute Kidney Injury In Cirrhosis Research Articles

Systematic Review and Meta-Analysis of Urine Neutrophil Gelatinase–Associated Lipocalin for Acute Kidney Injury in Cirrhosis

Systematic Review and Meta-Analysis of Urine Neutrophil Gelatinase–Associated Lipocalin for Acute Kidney Injury in Cirrhosis

13 Midodrine-Induced Urinary Retention as a Cause of Acute Kidney Injury in Cirrhosis: Not Always Hepatorenal But the Failed Therapy for it

13 Midodrine-Induced Urinary Retention as a Cause of Acute Kidney Injury in Cirrhosis: Not Always Hepatorenal But the Failed Therapy for it

Prospective validation of the EASL management algorithm for acute kidney injury in cirrhosis

The management of acute kidney injury (AKI) in cirrhosis is challenging. The EASL guidelines proposed an algorithm, but this has never been validated. We aimed to prospectively evaluate this algorithm in clinical practice. Prospective cohort study of consecutive hospitalized patients with cirrhosis and AKI. EASL management algorithm includes identification/treatment of precipitating factors, 2-day albumin infusion in patients with AKI ≥ stage 1B, and treatment with terlipressin in patients with hepatorenal syndrome (HRS-AKI). Primary outcome was treatment response, which included both full and partial response. Secondary outcomes were survival and adverse events associated with terlipressin therapy. A total of 202 AKI episodes in 139 patients were included. Overall treatment response was 80%, while renal replacement therapy was required in only 8%. Response to albumin infusion was achieved in 1/3 of episodes. Of patients not responding to albumin, most (74%) did not meet the diagnostic criteria of HRS-AKI, with ATN being the most common phenotype. Response rate in patients not meeting criteria of HRS-AKI was 70%. Only 30 patients met the diagnostic criteria HRS-AKI, and response rate to terlipressin was 61%. Median time from AKI diagnosis to terlipressin initiation was only 2.5 days. While urinary neutrophil gelatinase-associated lipocalin (uNGAL) could differentiate acute tubular necrosis (ATN) vs other phenotypes (AUROC 0.78), it did not predict response to therapy in HRS-AKI. Ninety-day transplant-free survival was negatively associated with MELD-Na, ATN and HRS-AKI as well as uNGAL. Three patients treated with terlipressin developed pulmonary edema. The application of the EASL AKI algorithm is associated with very good response rates and does not significantly delay initiation of terlipressin therapy.

Acute Kidney Injury and Hepatorenal Syndrome in Patients with Cirrhosis.

Acute kidney injury (AKI) is common in hospitalized patients with cirrhosis. Hepatorenal syndrome (HRS) is a type of AKI known as HRS-AKI. It is a severe complication of cirrhosis with high morbidity and mortality. While certain vasoconstrictor medications have been shown to improve HRS-AKI, no clear transplant-free survival benefit has been reported with medical therapies. Patients with HRS-AKI should be considered for urgent liver transplantation evaluation. In this review, we discuss the most recent updates on the definition, diagnosis, and management of AKI in cirrhosis, with special a emphasis on HRS.

Acute Kidney Injury in Critically Ill Cirrhotic Patients with Spontaneous Bacterial Peritonitis

Acute kidney injury (AKI) is an important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis (SBP). However, the definition of AKI in cirrhosis has been debated for many years. This study aims to compare the prediction accuracy of Kidney Disease: Improving Global Outcomes (KDIGO) and International Club of Ascites (ICA) criteria for hospital mortality in cirrhotic patients with SBP admitted to the intensive care unit (ICU).

Incidence and outcomes of acute kidney injury including hepatorenal syndrome in hospitalized patients with cirrhosis in the US

Acute kidney injury (AKI) in cirrhosis is common and associated with high morbidity, but the incidence rates of different etiologies of AKI are not well described in the US. We compared incidence rates, practice patterns, and outcomes across etiologies of AKI in cirrhosis. We performed a retrospective cohort study of 11 hospital networks, including consecutive adult patients admitted with AKI and cirrhosis in 2019. The etiology of AKI was adjudicated based on pre-specified clinical definitions (prerenal/hypovolemic AKI, hepatorenal syndrome [HRS-AKI], acute tubular necrosis [ATN], other). A total of 2,063 patients were included (median age 62 [IQR 54-69] years, 38.3% female, median MELD-Na score 26 [19-31]). The most common etiology was prerenal AKI (44.3%), followed by ATN (30.4%) and HRS-AKI (12.1%); 6.0% had other AKI, and 7.2% could not be classified. In our cohort, 8.1% of patients received a liver transplant and 36.5% died by 90 days. The lowest rate of death was observed in patients with prerenal AKI (22.2%; p <0.001), while death rates were higher but not significantly different from each other in those with HRS-AKI and ATN (49.0% vs. 52.7%; p= 0.42). Using prerenal AKI as a reference, the adjusted subdistribution hazard ratio (sHR) for 90-day mortality was higher for HRS-AKI (sHR 2.78; 95% CI 2.18-3.54; p <0.001) and ATN (sHR 2.83; 95% CI 2.36-3.41; p <0.001). In adjusted analysis, higher AKI stage and lack of complete response to treatment were associated with an increased risk of 90-day mortality (p <0.001 for all). AKI is a severe complication of cirrhosis. HRS-AKI is uncommon and is associated with similar outcomes to ATN. The etiology of AKI, AKI stage/severity, and non-response to treatment were associated with mortality. Further optimization of vasoconstrictors for HRS-AKI and supportive therapies for ATN are needed. Acute kidney injury (AKI) in cirrhosis carries high morbidity, and management is determined by the etiology of injury. However, a large and well-adjudicated multicenter database from US centers that uses updated AKI definitions is lacking. Our findings demonstrate that acute tubular necrosis and hepatorenal syndrome have similar outcomes (∼50% mortality at 90 days), though hepatorenal syndrome is uncommon (12% of all AKI cases). These findings represent practice patterns at US transplant/tertiary centers and can be used as a baseline, presenting the situation prior to the adoption of terlipressin in the US.

Acute Kidney Injury in Liver Cirrhosis.

Acute kidney injury (AKI) is common in cirrhotic patients affecting almost 20% of these patients. While multiple etiologies can lead to AKI, pre-renal azotemia seems to be the most common cause of AKI. Irrespective of the cause, AKI is associated with worse survival with the poorest outcomes observed in those with hepatorenal syndrome (HRS) and acute tubular necrosis (ATN). In recent years, new definitions, and classifications of AKI in cirrhosis have emerged. More knowledge has also become available regarding the benefits and drawbacks of albumin and terlipressin use in these patients. Diagnostic tools such as urinary biomarkers and point-of-care ultrasound (POCUS) became available and they will be used in the near future to differentiate between different causes of AKI and direct management of AKI in these patients. In this update, we will review these new classifications, treatment recommendations, and diagnostic tools for AKI in cirrhotic patients.

Acute Kidney Injury in Cirrhosis of Liver: it’s Clinical Spectrum and Association of Various Clinical Outcomes with Advancing Cirrhosis of the Liver

Background &amp; Objectives: Pakistan in tandem marks mortality of advance cirrhosis due to complications like hepatic encephalopathy, upper gastrointestinal bleeding and Acute kidney injury (AKI) contributing further morbidity and mortality. The study aimed to determine frequency, types and severity of AKI among cirrhotics and find association between AKI with various clinical outcomes among advance cirrhotics. Methods: All cirrhotics (both genders), age &gt; 18 years of various aetiologies with confirmed AKI were included and analysed retrospectively. Clinical, antiviral treatment and biochemical predictors of mortality in AKI were analysed by univariate regression however independent risk factors were analysed by multi regression (significant P values &lt; 0.05). Results: Out of 271 cirrhotics, 188 (69.37%) had AKI. Commonest to least common AKI pattern was pre-renal (59.5%), intrinsic (37.7%) post-renal (2.1%). Majority (45.2%) had international club of ascites (ICA-AKI) stage 3, (33.5%) ICA-AKI stage 2 and (21.3%) ICA-AKI stage 1. The overall mortality with AKI at 1,6 and 12 months were 12.8%, 39.1% and 54.3% respectively (significant p 0.001). Increased creatinine, international normalized ratio (INR), bilirubin, albumin, Child Turcotte Pugh (CTP) and Model of end stage liver disease (MELD) were in-hospital predictors of mortality where INR and albumin proved significant. Conclusion: AKI being frequent challenge among cirrhotics has commonest pattern as pre-renal with majority having severe AKI, ICA-Stage 3. Patients with AKI had higher mortality versus non-AKI. Rising creatinine, serum bilirubin, severity of cirrhosis (CTP and MELD score) were the significant predictors of in-hospital mortality where INR and albumin were most significant. Keywords: Acute kidney injury, international club of ascites, cirrhosis of liver, child Turcotte Pugh, International normalized ratio

Diagnostic and prognostic performance of urinary neutrophil gelatinase-associated lipocalin in patients with cirrhosis and acute kidney injury.

Acute kidney injury (AKI) commonly occurs in patients with decompensated cirrhosis. Urinary neutrophil gelatinase-associated lipocalin (uNGAL) could help discriminate between different etiologies of AKI. The aim of this study was to investigate the use of uNGAL in (1) the differential diagnosis of AKI, (2) predicting the response to terlipressin and albumin in patients with hepatorenal syndrome-AKI (HRS-AKI), and (3) predicting in-hospital mortality in patients with AKI. One hundred sixty-two consecutive patients with cirrhosis and AKI were included from 2015 to 2020 and followed until transplant, death, or 90 days. Standard urinary markers and uNGAL were measured. Data on treatment, type, and resolution of AKI were collected. Thirty-five patients (21.6%) had prerenal AKI, 64 (39.5%) HRS-AKI, 27 (16.7%) acute tubular necrosis-AKI (ATN-AKI), and 36 (22.2%) a mixed form of AKI. Mean values of uNGAL were significantly higher in ATN-AKI than in other types of AKI (1162 ng/ml [95% CI 423-2105 ng/ml] vs. 109 ng/ml [95% CI 52-192 ng/ml]; p < 0.001). uNGAL showed a high discrimination ability in predicting ATN-AKI (area under the receiver operating characteristic curve, 0.854; 95% CI 0.767-0.941; p < 0.001). The best-performing threshold was found to be 220 ng/ml (sensitivity, 89%; specificity, 78%). The same threshold was independently associated with a higher risk of nonresponse (adjusted OR [aOR], 6.17; 95% CI 1.41-27.03; p = 0.016). In multivariable analysis (adjusted for age, Model for End-Stage Liver Disease, acute-on-chronic liver failure, leukocytes, and type of AKI), uNGAL was an independent predictor of in-hospital mortality (aOR, 1.74; 95% CI 1.26-2.38; p = 0.001). uNGAL is an adequate biomarker for making a differential diagnosis of AKI in cirrhosis and predicting the response to terlipressin and albumin in patients with HRS-AKI. In addition, it is an independent predictor of in-hospital mortality.

Recent Advances in the Management of Hepatorenal Syndrome: A US Perspective

Acute kidney injury (AKI) is a common complication among decompensated patients with cirrhosis and is associated with significant mortality. 1 Garcia-Tsao G. Parikh C.R. Viola A. Acute kidney injury in cirrhosis. Hepatology. 2008; 48: 2064-2077 Crossref PubMed Scopus (441) Google Scholar In this setting, the most common phenotypes of AKI are hypovolemic/prerenal, acute tubular injury/necrosis, and hepatorenal syndrome (HRS). In this article, the most recent terminology put forth by the International Club of Ascites is used, HRS-AKI, which replaces the prior term HRS type 1. 2 Angeli P. Gines P. Wong F. et al. Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. Gut. 2015; 64: 531-537 Crossref PubMed Google Scholar HRS-AKI is a devastating complication of advanced cirrhosis occurring in approximately 17% of AKI cases 1 Garcia-Tsao G. Parikh C.R. Viola A. Acute kidney injury in cirrhosis. Hepatology. 2008; 48: 2064-2077 Crossref PubMed Scopus (441) Google Scholar and is associated with a high 90-day mortality rate of 45% to 51%. 3 Wong F. Pappas S.C. Curry M.P. et al. Terlipressin plus albumin for the treatment of type 1 hepatorenal syndrome. N Engl J Med. 2021; 384: 818-828 Crossref PubMed Scopus (86) Google Scholar ,4 Sanyal A.J. Boyer T.D. Frederick R.T. et al. Reversal of hepatorenal syndrome type 1 with terlipressin plus albumin vs. placebo plus albumin in a pooled analysis of the OT-0401 and REVERSE randomised clinical studies. Aliment Pharmacol Ther. 2017; 45: 1390-1402 Crossref PubMed Scopus (54) Google Scholar The pathophysiology of HRS-AKI is complex. 5 Biggins S.W. Angeli P. Garcia-Tsao G. et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021; 74: 1014-1048 Crossref PubMed Scopus (110) Google Scholar Because of portal hypertension, blood pools in the splanchnic circulation, leading to decreased effective arterial blood volume. As a result, endogenous vasoconstricting systems are activated, leading to sodium and water retention and decreased kidney perfusion. Overlapping with this process there also is increased gut permeability, bacterial translocation, and up-regulation of systemic inflammatory mediators, a secondary cascade that contributes further to impaired kidney perfusion and concomitantly leads to the functional kidney injury seen in HRS-AKI. These dynamic pathophysiologic changes could be potentiated further by infections, acute-on-chronic liver failure (ACLF), or variceal bleeding.

Novel Predictors of Contrast Induced Acute Kidney Injury in Cirrhosis

Novel Predictors of Contrast Induced Acute Kidney Injury in Cirrhosis

Prospective evaluation of the EASL clinical guidelines algorithm of management of acute kidney injury in cirrhosis

Prospective evaluation of the EASL clinical guidelines algorithm of management of acute kidney injury in cirrhosis

Predictors of mortality at 28-days in infection associated acute kidney injury in cirrhosis.

BACKGROUNDAcute kidney injury (AKI) in cirrhosis is important complication with poor outcomes. And infections are common cause for acute decompensation. Infections in cirrhosis lead to acute deterioration of hemodynamics leading to precipitation of AKI.AIMTo study predictors of mortality in patients with infection-associated AKI in cirrhosis.METHODSThis was a prospective, observational study conducted at tertiary care centre from January 2018 till April 2019. Total 119 participants with cirrhosis of liver presenting with AKI were included into the study. AKI was defined as per international club of Ascites-AKI criteria 2015. Patients were grouped into infection AKI and non-infection AKI. Non-infection AKI included patients with diuretic induced AKI and pre-renal AKI. Logistic regression analysis was used to determine predictors of mortality at 28-d.RESULTSOut of 119 patients, alcohol (n = 104) was most common etiology of cirrhosis. The infection AKI included 67 (56%) patients and non-infection AKI (n = 52) included pre-renal AKI in 36 (30%) and diuretic-induced AKI in 16 (14%) patients. Infection AKI had significantly higher bilirubin, higher international normalized ratio (INR), low serum sodium, higher total leukocyte count (TLC) and higher prevalence of hepatic encephalopathy (HE) as compared to non-infection AKI. Infection AKI had higher progression of AKI (19/67 vs 2/52; P = 0.01) and 28-d mortality (38/67 vs 4/5; P ≤ 0.01) as compared to non-infection AKI. At 28-d, non-survivors (n = 42) had significantly higher bilirubin, higher INR, low serum sodium, higher TLC and higher prevalence of HE as compared to survivors (n = 77). On subgroup analysis of Infection AKI group, on multivariate analysis, serum bilirubin as well as presence of HE were independent predictors of 28-d mortality. There was no significant difference of mortality at 90-d between two groups.CONCLUSIONInfection AKI in cirrhosis has a dismal prognosis with higher 28-d mortality as compared to non-infection AKI. Serum bilirubin and presence of HE predict 28-d mortality in infection AKI.

S3401 A Model to Predict Responsiveness to Vasoconstrictor Treatment in Acute Kidney Injury in Cirrhosis

Introduction: Acute kidney injury in cirrhosis is associated with high mortality. Therapy with vasoconstrictor and albumin leads to improvement in 40-50% of patients. Here we propose a predictive model, which can segregate the responders from non-responders, at the time of presentation. The non-responders could be referred early for liver transplant. Methods: In this study, 202 consecutive patients diagnosed with AKI in cirrhosis (using AKIN criteria) were selected for the study. The data was run through the proposed VGM model at the time of admission. The model included creatinine and MELD score in calculation. A value of >0.5 predicted response and ≤0.5 predicted non-response. The patients were started on vasoconstrictor therapy and albumin. The response to therapy was noted. Statistical analysis of the response was done and the result was represented as ROC curve, specificity and sensitivity were calculated. Results: Out of 202 patients, 131 patients (64.85%) were responders and 71 patients (35.14%) were non-responders to vasoconstrictor therapy. Non-responders had 100% mortality during followup. The predictive model had AUROC 0.737, sensitivity of 95% and specificity of 78% in predicting response to therapy. Conclusion: In a developing nation with limited resources, it would be highly beneficial both in terms of expenditure and to plan treatment, if there was a model to accurately predict the response to treatment with vasoconstrictors and albumin. It would probably help separate the subset of patients who are not likely to respond to treatment and refer them early for liver transplantation.

Perfusion Analysis of Kidney Injury in Rats With Cirrhosis Induced by Common Bile Duct Ligation Using Arterial Spin Labeling MRI.

Arterial spin labeling (ASL) has been proven to be effective in ischemia-induced acute kidney injury (AKI); however, validation of ASL magnetic resonance imaging (MRI) is limited in AKI in the presence of cirrhosis. To investigate the feasibility of ASL in revealing renal blood flow (RBF) changes in kidney injury in the presence of cirrhosis and to assess its value in the early diagnosis of disease. Longitudinal. Rats were randomized into baseline group (N = 3), sham surgery group (N = 18), and common bile duct ligation (BDL) group (N = 48). All groups were divided into six subgroups based on different sacrificed time points. 3 T scanner, prototypic pulsed ASL sequence using flow-sensitive alternating inversion recovery preparation, half-Fourier acquisition single-shot turbo spin echo sequence. RBF measurement was performed by ASL. Hematoxylin-eosin (HE) score, Hypoxia-inducible factor-1alpha (HIF-1α) score, peritubular capillar (PTC) density, alanine aminotransferase, aspartate aminotransferase, serum total bilirubin, total bile acids, serum creatinine (Scr), and blood urea nitrogen (BUN) were harvested. Analysis of variance, Pearson's correlation coefficient, and receiver operating characteristic curves were performed. P < 0.05 was considered statistically significant. RBF, HE score, HIF-1α score, and PTC density after BDL were significantly different from baseline. RBF was highly correlated with HE score, HIF-1α score, and PTC density (r = -0.7598, r = -0.7434, r = 0.6406, respectively). RBF and Scr began to differ significantly from baseline at day 3 and 7 after intervention, respectively. The areas under the curves of RBF, Scr, and BUN for distinguishing non-AKI from AKI in cirrhosis were 1.00, 0.888, and 0.911, while those for distinguishing mild from severe kidney injury were 0.961, 0.830, and 0.857, respectively. ASL allows the longitudinal assessment of the degree of AKI induced by cholestatic cirrhosis in rats and can serve as a noninvasive marker for the early and accurate diagnosis of AKI. 2 TECHNICAL EFFICACY STAGE: 2.

Metabolomics to Predict Acute Kidney Injury in Cirrhosis

Patients with cirrhosis have a high risk of developing acute kidney injury (AKI), which is associated with a poor short-term survival and a high healthcare burden (1). Almost half of inpatients develop AKI during hospitalization and nearly 20% of AKI episodes are nosocomial(2). It is well known that AKI in most patients with cirrhosis is related to the underlying circulatory dysfunction due to splanchnic arterial vasodilation, reduction of effecting circulating volume, and renal hypoperfusion(1).

Current knowledge about biomarkers of acute kidney injury in liver cirrhosis.

Acute kidney injury (AKI) is common in advanced cirrhosis. Prerenal azotemia, hepatorenal syndrome, and acute tubular necrosis are the main causes of AKI in patients with cirrhosis. Evaluation of renal function and differentiation between functional and structural kidney injury are important issues in the management of cirrhosis. However, AKI in cirrhosis exists as a complex clinical spectrum rather than concrete clinical entity. Based on current evidence, changes in serum creatinine (Cr) levels remain the most appropriate standard for defining AKI in cirrhosis. However, serum Cr has a limited role in assessing renal function in this population. This review examines previous studies that investigated the ability of recent biomarkers for AKI in cirrhosis from the perspective of earlier and accurate diagnosis, classification of AKI phenotype, and prediction of clinical outcomes. Serum cystatin C and urine neutrophil gelatinase-associated lipocalin have been extensively studied in cirrhosis, and have facilitated improved diagnosis and prognosis prediction in patients with AKI. In addition, urine N-acetyl-β-D-glucosaminidase, interleukin 18, and kidney injury molecule 1 are other promising biomarkers for advanced cirrhosis. However, the clinical significance of these markers remains unclear because there are no cut-off values defining the normal range and differentiating phenotypes of AKI. In addition, AKI has been defined in terms of serum Cr, and renal biopsy—the gold standard—has not been carried out in most studies. Further discovery of innovate biomarkers and incorporation of various markers could improve the diagnosis and prognosis prediction of AKI, and will translate into meaningful improvements in patient outcomes.

Acute kidney injury and hepatorenal syndrome in cirrhosis.

Acute kidney injury (AKI) in cirrhosis, including hepatorenal syndrome (HRS), is a common and serious complication in cirrhotic patients, leading to significant morbidity and mortality. AKI is separated into two categories, non-HRS AKI and HRS-AKI. The most recent definition and diagnostic criteria of AKI in cirrhosis and HRS have helped diagnose and prognosticate the disease. The pathophysiology behind non-HRS-AKI and HRS is more complicated than once theorized and involves more processes than just splanchnic vasodilation. The common biomarkers clinicians use to assess kidney injury have significant limitations in cirrhosis patients; novel biomarkers being studied have shown promise but require further studies in clinical settings and animal models. The overall management of non-HRS AKI and HRS-AKI requires a systematic approach. Although pharmacological treatments have shown mortality benefit, the ideal HRS treatment option is liver transplantation with or without simultaneous kidney transplantation. Further research is required to optimize pharmacologic and nonpharmacologic approaches to treatment. This article reviews the current guidelines and recommendations of AKI in cirrhosis.

Urinary NGAL as a Diagnostic and Prognostic Marker for Acute Kidney Injury in Cirrhosis: A Prospective Study.

INTRODUCTION:Urinary neutrophil gelatinase-associated lipocalin (NGAL) has shown promise in differentiating acute tubular necrosis (ATN) from other types of acute kidney injuries (AKIs) in cirrhosis, particularly hepatorenal syndrome (HRS). However, NGAL is not currently available in clinical practice in North America.METHODS:Urinary NGAL was measured in a prospective cohort of 213 US hospitalized patients with decompensated cirrhosis (161 with AKI and 52 reference patients without AKI). NGAL was assessed for its ability to discriminate ATN from non-ATN AKI and to predict 90-day outcomes.RESULTS:Among patients with AKI, 57 (35%) had prerenal AKI, 55 (34%) had HRS, and 49 (30%) had ATN, with a median serum creatinine of 2.0 (interquartile range 1.5, 3.0) mg/dL at enrollment. At an optimal cutpoint of 244 μg/g creatinine, NGAL distinguished ATN (344 [132, 1,429] μg/g creatinine) from prerenal AKI (45 [0, 154] μg/g) or HRS (110 [50, 393] μg/g; P < 0.001), with a C statistic of 0.762 (95% confidence interval 0.682, 0.842). By 90 days, 71 of 213 patients (33%) died. Higher median NGAL was associated with death (159 [50, 865] vs 58 [0, 191] μg/g; P < 0.001). In adjusted and unadjusted analysis, NGAL significantly predicted 90-day transplant-free survival (P < 0.05 for all Cox models) and outperformed Model for End-Stage Liver Disease score by C statistic (0.697 vs 0.686; P = 0.04), net reclassification index (37%; P = 0.008), and integrated discrimination increment (2.7%; P = 0.02).DISCUSSION:NGAL differentiates the type of AKI in cirrhosis and may improve prediction of mortality; therefore, it holds potential to affect management of AKI in cirrhosis.

Royal Free Hospital-estimated glomerular filtration rate for prognostic stratification of first acute kidney injury in cirrhosis.

Renal function is a major determinant of prognosis in patients with cirrhosis. Current guidelines only contemplate serum creatinine (sCr) to assess kidney injury. However, there are formulas to estimate glomerular filtration rate (eGFR) which better measure renal function in patients listed for liver transplantation. There is no data available on whether these formulas predict prognosis in patients with acute kidney injury (AKI). In 143 patients presenting with a first episode of AKI, we compared the prognostic value of renal function estimated using sCr or eGFR assessed with Modification of Diet in Renal Disease (MDRD-6), chronic kidney disease epidemiology (CKD-EPI) and Royal Free Hospital (RFH) for renal replacement therapy (RRT) within 30days of AKI, and 30- and 90-day transplant-free survival. eGFR was calculated on values obtained before and at admission, at presentation of AKI (D0) and 48hours after AKI (D2).15% of patients (more commonly in alcohol+metabolic etiology; P=.049 vs other) required RRT. Transplant-free survival at 30-and 90-day were 77% and 63%. Among sCr, MDRD-6, CKD-EPI and RFH-eGFR, the latter predicted best RRT (HR 0.937 95% CI 0.893-0.982, P=.007), 30-d (HR 0.936 95% CI 0.901-0.972, P=.001) and 90-d (HR 0.934 95% CI 0.908-0.972, P<.001) mortality/OLT. Renal function estimated using the RFH-eGFR calculated at D2 after AKI diagnosis is a strong predictor of RRT and of 30-d and 90-d transplant-free survival. Results suggest that in cirrhosis, RFH-eGFR may be a better indicator of prognosis in AKI than sCr.