The diagnosis and management of nonalcoholic fatty liver disease: A patient-friendly summary of the 2018 AASLD guidelines.

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Center Variation in Intention-to-Treat Survival Among Patients Listed for Liver Transplant.

In the United States, centers performing liver transplant (LT) are primarily evaluated by patient survival within 1 year after LT, but tight clustering of outcomes allows only a narrow window for evaluation of center variation for quality improvement. Alternate measures more relevant to patients and the transplant community are needed. We examined adults listed for LT in the United States, using data submitted to the Scientific Registry of Transplant Recipients. Intention-to-treat (ITT) survival was defined as survival within 1 year from listing, regardless of transplant. Mixed effects/frailty models were used to assess center variation in ITT survival. Between January 2010 and December 2016, there were 66,428 new listings at 113 centers. Overall, median 1-year ITT survival was 79.8% (interquartile range [IQR], 76.1%-83.4%), whereas 1-year waiting-list (WL) survival was 75.8% (IQR, 71.2%-79.4%), and 1-year post-LT survival was 90.0% (IQR, 87.9%-91.8%). Higher rates of ITT mortality were correlated with increased WL mortality (correlation, r = 0.76), increased post-LT mortality (r = 0.31), lower volume centers (r = -0.34), and lower transplant rate ratio (r = -0.25). Similar patterns were observed in the subgroup of WL candidates listed with Model for End-Stage Liver Disease (MELD) ≥25: median 1-year ITT survival was 65.2% (IQR, 60.2%-72.6%), whereas 1-year post-LT survival was 87.5% (IQR, 84.0%-90.9%), and 1-year WL survival was 36.6% (IQR, 27.9%-47.0%). In mixed effects modeling, the transplant center was an independent predictor of ITT survival even after adjustment for age, sex, MELD, and sociodemographic variables. Center variation for ITT survival was larger compared with post-LT survival. The measurement of ITT outcome offers a complementary method to assess center performance. This is a first step toward understanding differences in program quality beyond patient and graft survival after LT.

Model for End-Stage Liver Disease-Lactate and Prediction of Inpatient Mortality in Patients With Chronic Liver Disease.

BACKGROUND AND AIMS: Compared to other chronic diseases, patients with chronic liver disease (CLD) have significantly higher inpatient mortality; accurate models to predict inpatient mortality are lacking. Serum lactate (LA) may be elevated in patients with CLD due to both tissue hypoperfusion as well as decreased LA clearance. We hypothesized that a parsimonious model consisting of Model for End-Stage Liver Disease (MELD) and LA at admission may predict inpatient mortality in patients with CLD. APPROACH AND RESULTS: We examined all patients with CLD in two large and diverse health care systems in Texas (North Texas [NTX] and Central Texas [CTX]) between 2010 and 2015. We developed (n = 3,588) and validated (n = 1,804) a model containing MELD and LA measured at the time of hospitalization. We further validated the model in a second cohort of 14 tertiary care hepatology centers that prospectively enrolled nonelective hospitalized patients with cirrhosis (n = 726). MELD-LA was an excellent predictor of inpatient mortality in development (concordance statistic [C-statistic] = 0.81, 95% confidence interval [CI] 0.79-0.82) and both validation cohorts (CTX cohort, C-statistic = 0.85, 95% CI 0.78-0.87; multicenter cohort C-statistic = 0.82, 95% CI 0.74-0.88). MELD-LA performed especially well in patients with specific cirrhosis diagnoses (C-statistic = 0.84, 95% CI 0.81-0.86) or sepsis (C-statistic = 0.80, 95% CI 0.78-0.82). For MELD score 25, inpatient mortality rates were 11.2% (LA = 1 mmol/L), 19.4% (LA = 3 mmol/L), 34.3% (LA = 5 mmol/L), and >50% (LA > 8 mmol/L). A linear increase (P < 0.01) was seen in MELD-LA and increasing number of organ failures. Overall, use of MELD-LA improved the risk prediction in 23.5% of patients compared to MELD alone. CONCLUSIONS: MELD-LA (bswh.md/meldla) is an early and objective predictor of inpatient mortality and may serve as a model for risk assessment and guide therapeutic options.

A Model for Glomerular Filtration Rate Assessment in Liver Disease (GRAIL) in the Presence of Renal Dysfunction.

Estimation of glomerular filtration rate (eGFR) in patients with liver disease is suboptimal in the presence of renal dysfunction. We developed a model for GFR assessment in liver disease (GRAIL) before and after liver transplantation (LT). GRAIL was derived using objective variables (creatinine, blood urea nitrogen, age, gender, race, and albumin) to estimate GFR based on timing of measurement relative to LT and degree of renal dysfunction (www.bswh.md/grail). The measured GFR (mGFR) by iothalamate clearance (n = 12,122, 1985-2015) at protocol time points before/after LT was used as reference. GRAIL was compared with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD-4, MDRD-6) equations for mGFR < 30 mL/min/1.73 m2 . Prediction of development of chronic kidney disease (mGFR < 20 mL/min/1.73 m2 , initiation of chronic dialysis) and listing or receipt of kidney transplantation within 5 years was examined in internal cohort (n = 785) and external validation (n = 68,217, 2001-2015). GRAIL had less bias and was more accurate and precise as compared with CKD-EPI, MDRD-4, and MDRD-6 at time points before/after LT for low GFR. For mGFR < 30 mL/min/1.73 m2 , the median difference (eGFR-mGFR) was GRAIL: 5.24 (9.65) mL/min/1.73 m2 as compared with CKD-EPI: 8.70 (18.24) mL/min/1.73 m2 , MDRD-4: 8.82 (17.38) mL/min/1.73 m2 , and MDRD-6: 6.53 (14.42) mL/min/1.73 m2 . Before LT, GRAIL correctly classified 75% as having mGFR < 30 mL/min/1.73 m2 versus 36.1% (CKD-EPI), 36.1% (MDRD-4), and 52.8% (MDRD-6) (P < 0.01). An eGFR < 30 mL/min/1.73 m2 by GRAIL predicted development of CKD (26.9% versus 4.6% CKD-EPI, 5.9% MDRD-4, and 10.5% MDRD-6) in center data and needing kidney after LT (48.3% versus 22.0% CKD-EPI versus 23.1% MDRD-4 versus 48.3% MDRD-6, P < 0.01) in national data within 5 years after LT. Conclusion: GRAIL may serve as an alternative model to estimate GFR among patients with liver disease before and after LT at low GFR.

Multicenter analysis of the use of transjugular intrahepatic portosystemic shunt for management of MPN-associated portal hypertension.

BCR-ABL1-negative myeloproliferative neoplasms (MPNs) are clonal stem cell disorders defined by proliferation of one or more myeloid lineages, and carry an increased risk of vascular events and progression to myelofibrosis and leukemia. Portal hypertension (pHTN) occurs in 7-18% of MPN patients via both thrombotic and nonthrombotic mechanisms and portends a poor prognosis. Transjugular intrahepatic portosystemic shunt (TIPS) has been used in the management of MPN-associated pHTN; however, data on long-term outcomes of TIPS in this setting is limited and the optimal management of medically refractory MPN-associated pHTN is not known. In order to assess the efficacy and long-term outcomes of TIPS in MPN-associated pHTN, we performed a retrospective analysis of 29 MPN patients who underwent TIPS at three academic medical centers between 1997 and 2016. The majority of patients experienced complete clinical resolution of pHTN and its clinical sequelae following TIPS. One, two, three, and four-year overall survival post-TIPS was 96.4%, 92.3%, 84.6%, and 71.4%, respectively. However, despite therapeutic anticoagulation, in-stent thrombosis occurred in 31.0% of patients after TIPS, necessitating additional interventions. In conclusion, TIPS can be an effective intervention for MPN-associated pHTN regardless of etiology. However, TIPS thrombosis is a frequent complication in the MPN population and indefinite anticoagulation post-TIPS should be considered.

Daclatasvir combined with sofosbuvir or simeprevir in liver transplant recipients with severe recurrent hepatitis C infection.

Daclatasvir (DCV) is a potent, pangenotypic nonstructural protein 5A inhibitor with demonstrated antiviral efficacy when combined with sofosbuvir (SOF) or simeprevir (SMV) with or without ribavirin (RBV) in patients with chronic hepatitis C virus (HCV) infection. Herein, we report efficacy and safety data for DCV-based all-oral antiviral therapy in liver transplantation (LT) recipients with severe recurrent HCV. DCV at 60 mg/day was administered for up to 24 weeks as part of a compassionate use protocol. The study included 97 LT recipients with a mean age of 59.3 ± 8.2 years; 93% had genotype 1 HCV and 31% had biopsy-proven cirrhosis between the time of LT and the initiation of DCV. The mean Model for End-Stage Liver Disease (MELD) score was 13.0 ± 6.0, and the proportion with Child-Turcotte-Pugh (CTP) A/B/C was 51%/31%/12%, respectively. Mean HCV RNA at DCV initiation was 14.3 × 6 log10 IU/mL, and 37% had severe cholestatic HCV infection. Antiviral regimens were selected by the local investigator and included DCV+SOF (n = 77), DCV+SMV (n = 18), and DCV+SMV+SOF (n = 2); 35% overall received RBV. At the end of treatment (EOT) and 12 weeks after EOT, 88 (91%) and 84 (87%) patients, respectively, were HCV RNA negative or had levels <43 IU/mL. CTP and MELD scores significantly improved between DCV-based treatment initiation and last contact. Three virological breakthroughs and 2 relapses occurred in patients treated with DCV+SMV with or without RBV. None of the 8 patient deaths (6 during and 2 after therapy) were attributed to therapy. In conclusion, DCV-based all-oral antiviral therapy was well tolerated and resulted in a high sustained virological response in LT recipients with severe recurrent HCV infection. Most treated patients experienced stabilization or improvement in their clinical status.

Outcomes in pediatric hepatitis C transplant recipients: analysis of the UNOS database.

HCV may lead to the development of ESLD in late childhood and, consequently, contributes to the need for liver transplantation. The aim of this study was to examine post-transplant outcomes in HCV-positive pediatric patients with ESLD from any cause and to determine the impact of the PELD scoring system, introduced in February 2002, on post-transplant patient and graft survival. A retrospective analysis of the UNOS database from 1994 to 2010 was performed to assess graft and patient survival in pediatric HCV-seropositive liver transplant recipients. Graft survival and patient survival comparing subjects in the pre-PELD era and post-PELD era were analyzed using Kaplan-Meier statistics. Factors associated with survival were identified using Cox regression analysis. Of 120 pediatric HCV transplant recipients, 80 were transplanted in the pre-PELD era and 40 were transplanted post-PELD. Median serum total bilirubin, INR, and creatinine were 4.8 mg/dL, 1.6, and 0.7 mg/dL in the pre-PELD era vs. 5.5 mg/dL, 1.7, and 0.6 mg/mL, respectively, in the post-PELD era (p NS). One-yr graft survival in the pre-PELD vs. post-PELD era was 65.0% and 89.7%, respectively (p < 0.01); corresponding three-yr graft survival was 57.3% vs. 76.2% (p = 0.04). One-yr patient survival in the pre-PELD vs. post-PELD era was 79.0% and 97.5%, respectively (p < 0.01); corresponding three-yr survival was 79.0% vs. 89.4% (p = 0.17). Twenty-eight patients (23.3%) were retransplanted: 24 (30%) in the pre-PELD era (median time to retransplant 272 days) and four (10%) in the post-PELD era (median time to retransplant 586 days). Early follow-up demonstrates a trend toward improved pediatric HCV liver transplant graft and patient survival in the post-PELD era. Superior outcomes may be attributed to pretransplant factors, improved surgical technique and better treatment options for HCV infection.

Drug-induced liver injury due to cancer chemotherapeutic agents.

Drug-induced liver injury (DILI) due to chemotherapeutic drugs is a significant cause of morbidity and mortality. Most cases of chemotherapy-induced hepatotoxicity are idiosyncratic and do not have a unique clinical or histological signature that is distinct from other agents that cause DILI. The major mechanisms underlying chemotherapy-related hepatotoxicity are based on the production of reactive metabolites generated by phase I oxidation reactions, immunological injury, or alterations in mitochondrial function. Underlying liver disease and hepatic involvement by tumor are important modifiers of liver injury, and reversibility is not universal after drug cessation. Chemotherapy can also exacerbate underlying liver disease, particularly hepatitis B, leading to worsening hepatic function. Diagnosing DILI due to chemotherapeutic agents is particularly challenging because competing etiologies, such as hepatotoxicity from other medications, opportunistic infections, radiation therapy, and pre-existing liver disease, are frequent.

End-stage renal disease after liver transplantation in patients with pre-transplant chronic kidney disease.

UNLABELLED: Renal dysfunction prior to liver transplantation has a marked impact on post-transplant kidney outcomes. AIM: The aim of this study was to assess post-transplant renal function in patients with chronic kidney disease (CKD) receiving orthotopic liver transplantation (OLT) alone. METHODS: Retrospective review of 40 OLT recipients with pre-transplant CKD (serum creatinine ≥2 mg/dL for at least three months) at the University of Pennsylvania from February 2002 to July 2010. Primary outcome was estimated glomerular filtration rate (eGFR) up to three years post-transplant. Secondary outcomes included incidence of stage 4 CKD (eGFR < 30 mL/min), need for renal replacement therapy (RRT), meeting criteria for kidney transplant listing (eGFR ≤ 20 mL/min), and mortality. RESULTS: Median patient age was 56.5 yr and 48% patients had pre-transplant diabetes. Median serum creatinine at transplant was 2.7 mg/dL (eGFR = 24 mL/min). Median eGFR at one, two, and three yr post-transplant was 35, 34, and 37 mL/min, respectively. Twelve patients (30%) required RRT at a median of 1.21 yr post-transplant and 16 (40%) achieved an eGFR ≤ 20 mL/min at 1.09 yr post-transplant. Mortality was 35% at a median of 1.60 years post-transplant. CONCLUSIONS: OLT recipients with pre-transplant CKD have a substantial burden of post-transplant renal dysfunction and high short-term mortality, questioning the rationale for OLT alone in this population.

Factors that predict short-term intensive care unit mortality in patients with cirrhosis.

BACKGROUND & AIMS: Despite advances in critical care medicine, the mortality rate is high among critically ill patients with cirrhosis. We aimed to identify factors that predict early (7 d) mortality among patients with cirrhosis admitted to the intensive care unit (ICU) and to develop a risk-stratification model. METHODS: We collected data from patients with cirrhosis admitted to the ICU at Indiana University (IU-ICU) from December 1, 2006, through December 31, 2009 (n = 185), or at the University of Pennsylvania (Penn-ICU) from May 1, 2005, through December 31, 2010 (n = 206). Factors associated with mortality within 7 days of admission (7-d mortality) were determined by logistic regression analyses. A model was constructed based on the predictive parameters available on the first day of ICU admission in the IU-ICU cohort and then validated in the Penn-ICU cohort. RESULTS: Median Model for End-stage Liver Disease (MELD) scores at ICU admission were 25 in the IU-ICU cohort (interquartile range, 23-34) and 32 in the Penn-ICU cohort (interquartile range, 26-41); corresponding 7-day mortalities were 28.3% and 53.6%, respectively. MELD score (odds ratio, 1.13; 95% confidence interval [CI], 1.07-1.2) and mechanical ventilation (odds ratio, 5.7; 95% CI, 2.3-14.1) were associated independently with 7-day mortality in the IU-ICU. A model based on these 2 variables separated IU-ICU patients into low-, medium-, and high-risk groups; these groups had 7-day mortalities of 9%, 27%, and 74%, respectively (concordance index, 0.80; 95% CI, 0.72-0.87; P < 10(-8)). The model was applied to the Penn-ICU cohort; the low-, medium-, and high-risk groups had 7-day mortalities of 33%, 56%, and 71%, respectively (concordance index, 0.67; 95% CI, 0.59-0.74; P < 10(-4)). CONCLUSIONS: A model based on MELD score and mechanical ventilation on day 1 can stratify risk of early mortality in patients with cirrhosis admitted to the ICU. More studies are needed to validate this model and to enhance its clinical utility.

Chronic kidney disease after liver transplantation in human immunodeficiency virus/hepatitis C virus-coinfected recipients versus human immunodeficiency virus-infected recipients without hepatitis C virus: results from the National Institutes of Health multi-site study.

Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) are both associated with chronic kidney disease (CKD), a major complication after orthotopic liver transplantation (OLT). The aim of this study was to assess predictors of post-OLT CKD in HIV/HCV-coinfected recipients versus HIV-infected recipients without HCV (HIV/non-HCV recipients). Data from a National Institutes of Health study of 116 OLT recipients (35 HIV/non-HCV recipients and 81 HIV/HCV-coinfected recipients) from 2003 to 2010 (Solid Organ Transplantation in HIV: Multi-Site Study) were analyzed for the pretransplant CKD prevalence [estimated glomerular filtration rate (eGFR) < 60 mL/minute for ≥3 months] and the incidence of CKD up to 3 years posttransplant. Proportional hazards models were performed to assess predictors of posttransplant CKD. A contemporaneous cohort of HCV-monoinfected transplant recipients from the Scientific Registry of Transplant Recipients database was also analyzed. The median age at transplant was 48 years, the median serum creatinine level was 1.1 mg/dL, and the median eGFR was 77 mL/minute. Thirty-four patients were suspected to have pretransplant CKD; 20 of these patients (59%) had posttransplant CKD. Among the 82 patients without pretransplant CKD (26 HIV/non-HCV patients and 56 HIV/HCV-coinfected patients), the incidence of stage 3 CKD 3 years after OLT was 62% (55% of HIV/non-HCV patients and 65% of HIV/HCV-coinfected patients), and the incidence of stage 4/5 CKD was 8% (0% of HIV/non-HCV patients and 12% of HIV/HCV-coinfected patients). In a multivariate analysis, older age [[hazard ratio (HR) = 1.05 per year, P = 0.03] and the CD4 count (HR = 0.90 per 50 cells/µL, P = 0.01) were significant predictors of CKD. HCV coinfection was significantly associated with stage 4/5 CKD (HR = 10.8, P = 0.03) after adjustments for age. The cumulative incidence of stage 4/5 CKD was significantly higher for HIV/HCV-coinfected patients versus HIV/non-HCV transplant recipients and HCV-monoinfected transplant recipients (P = 0.001). In conclusion, CKD occurs frequently in HIV-infected transplant recipients. Predictors of posttransplant CKD include older age and a lower posttransplant CD4 count. HCV coinfection is associated with a higher incidence of stage 4/5 CKD.

Acute-on-chronic liver failure before liver transplantation: impact on posttransplant outcomes.

BACKGROUND: Acute decompensation in patients with chronic liver disease, resulting from acute kidney injury and infections, leads to significant morbidity and mortality. It is unclear whether patients who develop acute-on-chronic liver failure (ACLF) have poor outcomes after liver transplantation. METHODS: We performed a single-center retrospective cohort study of 332 patients to evaluate the effect of ACLF, defined as an acute rise in the Model for End-Stage Liver Disease score of more than 5 within 4 weeks before transplantation, on posttransplant outcomes including stage 4 chronic kidney disease, death, recurrent cirrhosis, or graft failure requiring retransplantation. RESULTS AND CONCLUSIONS: One hundred fifty-seven patients in the study had ACLF and 175 patients had no ACLF (non-ACLF) pretransplant. Thirty-four patients in the entire cohort received dual organs, 10 of them (29.4%) had ACLF. Seventy-six percent of the patients with ACLF had acute kidney injury as their reason for decompensation and 23.6% had an infection. Mean Model for End-Stage Liver Disease score at transplant was significantly different between the groups (ACLF 28.77 vs. non-ACLF 21.23, P<0.0001). A total of 16.6% of the patients achieved an estimated glomerular filtration rate (eGFR) less than 30 mL/min, 21% of patients died, 12.3% developed cirrhosis, and 7.5% received a second transplant. There was no difference in mean eGFR between the ACLF and non-ACLF cohorts at 3 years posttransplant (56.35 mL/min vs. 59.93 mL/min, respectively, P=0.27). On multivariate analysis, ACLF was not significantly associated with eGFR less than 30 mL/min, death, recurrent cirrhosis, or retransplantation when adjusted for potential confounders.

Chronic kidney disease after orthotopic liver transplantation: impact of hepatitis C infection.

BACKGROUND: Hepatitis C virus (HCV) infection has been shown to be a potential risk factor for the development of chronic kidney disease in liver transplant recipients. METHODS: We performed a retrospective cohort study of 307 patients with and without HCV cirrhosis and preserved pretransplant renal function (serum creatinine<1.5 mg/dL pretransplantation) to assess the impact of HCV on the incidence of posttransplant chronic kidney disease. Kaplan-Meier analysis was performed for time to development of estimated glomerular filtration rate (eGFR) less than 30 mL/min, need for dialysis, and mortality. RESULTS: One hundred eighty-one patients were transplanted for HCV cirrhosis and 126 recipients had other causes of liver disease. Mean model for end-stage liver disease scores were 21.64 in the HCV group and 21.30 in the non-HCV group (P=0.58); 51% of patients in the HCV cohort had hepatocellular carcinoma compared with 27% in the non-HCV cohort (P<0.001). Mean pretransplant serum creatinine level was 0.89 mg/dL in both groups. At 3 years posttransplant, eGFR did not differ between the HCV and non-HCV cohorts (64.96 mL/min vs. 66.09 mL/min; P=0.71). A total of 14.4% of the patients with HCV achieved an eGFR less than 30 mL/min compared with 10.3% of the patients without HCV (P=0.13). There was no difference between the cohorts with respect to requirement for dialysis (P=0.73) or deaths (P=0.08), including those that were liver related (P=0.15). CONCLUSIONS: Patients with HCV cirrhosis and normal preliver transplant renal function do not have worse posttransplant renal outcomes compared with those with other causes of liver disease.

Outcomes after liver transplantation: chronic kidney disease.

1. Chronic kidney disease is a common complication after liver transplantation and has a major impact on graft and patient survival. 2. Pretransplant renal dysfunction is the most important determinant of posttransplant chronic kidney disease; other factors include the presence of diabetes/hypertension, acute kidney injury pre-transplant and post-transplant, and the use of calcineurin inhibitor-based immunosuppression. 3. The most common cause of end-stage renal disease post-orthotopic liver transplantation is calcineurin inhibitor toxicity, and this emphasizes the need for calcineurin inhibitor minimization protocols post-transplant. 4. The presence of chronic kidney disease post-orthotopic liver transplantation not only is important with respect to the need for renal replacement therapy and kidney transplantation but also increases cardiovascular risk dramatically. 5. The Model for End-Stage Liver Disease score is partly driven by creatinine, and it is not uncommon to have an elevated creatinine level in those who have a high Model for End-Stage Liver Disease score and are close to having an organ allocated. Thus, evaluating patients with advanced liver disease and pretransplant acute kidney injury is challenging. It is important to identify pre-liver transplant patients at high risk for early evolution of chronic kidney disease post-transplant in order to appropriately select patients for combined liver/kidney transplantation.

Transplantation: impact of pretransplant renal insufficiency.

Pre-liver transplant renal dysfunction is associated with decreased survival following transplantation and is also a prognostic indicator of posttransplant chronic kidney disease. Selection of patients for combined liver/kidney transplantation versus orthotopic liver transplantation alone (OLTa) is often difficult given the lack of a reliable method to predict which patients will have ongoing severe renal dysfunction in the absence of concomitant kidney transplantation. We hypothesized that most patients with pretransplant renal dysfunction (serum creatinine > or = 1.5 mg/dL for at least 2 weeks prior to and at time of transplant) will not experience a rapid decline in estimated glomerular filtration rates (eGF) post-OLTa to the point of necessitating consideration for kidney transplantation, even in the setting of calcineurin inhibitor-based immunosuppression. We performed a single-center retrospective study of 60 OLTa patients with pretransplant renal dysfunction transplanted between 2000 and 2005. Kaplan-Meier analysis was performed of the time interval to develop eGFR < 20 mL/minute post-OLTa. At OLTa, the mean patient age was 59 years, and median serum creatinine was 1.8 mg/dL; 42% patients were hepatitis C-positive, 32% were diabetic, 38% had kidney dysfunction > 12 weeks, and 5% were receiving hemodialysis. After 36 months median follow-up post-OLTa, only 8 patients (13%) with significant renal dysfunction pre-OLTa achieved eGFR < 20 mL/minute. Patients with pretransplant kidney dysfunction > 12 weeks were at increased risk for eGFR < 20 mL/minute (hazard ratio = 5.3, P = 0.04), a risk that escalated after adjustment for age and serum creatinine at transplant (hazard ratio = 8.9, P = 0.01). Significant predictors of eGFR < 20 mL/minute post-OLTa in this patient cohort were the presence of diabetes and the serum creatinine level at transplant. In conclusion, few patients with preexisting renal dysfunction, especially if <12 weeks duration, experience a significant drop in eGFR post-OLTa.