Post–Liver Transplant Early Allograft Dysfunction Modifies the Effect of Pre–Liver Transplant Renal Dysfunction on Post–Liver Transplant Survival

Abstract

Pre-liver transplantation (LT) renal dysfunction is associated with poor post-LT survival. We studied whether early allograft dysfunction (EAD) modifies this association. Data on 2,856 primary LT recipients who received a transplant between 1998 and 2018 were retrospectively reviewed. Patients who died within the first post-LT week or received multiorgan transplants and previous LT recipients were excluded. EAD was defined as (1) total bilirubin ≥ 10 mg/dL on postoperative day (POD) 7, (2) international normalized ratio ≥1.6 on POD 7, and/or (3) alanine aminotransferase or aspartate aminotransferase ≥2000 IU/mL in the first postoperative week. Pre-LT renal dysfunction was defined as serum creatinine >1.5 mg/dL or on renal replacement therapy at LT. Patients were divided into 4 groups according to pre-LT renal dysfunction and post-LT EAD development. Recipients who had both pre-LT renal dysfunction and post-LT EAD had the worst unadjusted 1-year, 3-year, and 5-year post-LT patient and graft survival, whereas patients who had neither renal dysfunction nor EAD had the best survival (P < 0.001). After adjusting for multiple factors, the risk of death was significantly higher only in those with both pre-LT renal dysfunction and post-LT EAD (adjusted hazard ratio [aHR], 2.19; 95% confidence interval [CI], 1.58-3.03; P < 0.001), whereas those with renal dysfunction and no EAD had a comparable risk of death to those with normal kidney function at LT (aHR, 1.12; 95% CI, 0.86-1.45; P = 0.41). Results remained unchanged when pre-LT renal dysfunction was redefined using different glomerular filtration rate cutoffs. Pre-LT renal dysfunction negatively impacts post-LT survival only in patients who develop EAD. Livers at higher risk of post-LT EAD should be used with caution in recipients with pre-LT renal dysfunction.

Donor’s seral creatinine as a predictor of early allograft dysfunction after liver transplantation: A retrospective cohort study with propensity score analysis

“…Seral creatinine is the most commonly used indicator of kidney function for estimated glomerular ltration rate (eGFR) by evaluating the endogenous creatinine clearance [8]. Previous studies have focused on the effects of recipients' pre-and posttransplant renal dysfunction with increased seral creatinine on the survival outcomes [9,10]. In this study, we interestingly found that the seral creatinine of donors was higher in patients with EAD after DCD liver transplantation.…”

“…EAD was a critical condition after liver transplantation, contributing to increased complication rates, and subsequent impaired posttransplant survival. The incidence of EAD ranges from 20-40% in recipients after LT, according to the variant de nition and criteria of EAD [4,12,[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. In this study, we adopted the EAD criteria developed by Olthoff in 2010 [12], which was the most acceptable EAD de nition in MELD era, and de ned by elevation of ALT, AST, INR or bilirubin within 7 days after LT. Undoubtably, recipients diagnosed with EAD had a higher probability of increased post-transplant complications, prolonged intensive care unit stays, delayed discharge, and graft failure [6,12].…”

A meta‐analysis on the prevalence of chronic kidney disease in liver transplant candidates and its associated risk factors and outcomes

“…However, the development of chronic kidney disease (CKD) before liver transplant persists as a complicated, multifaceted issue leading to a multitude of adverse outcomes including inferior graft survival, increased infection, increased health care cost, and longer duration of stay [3][4][5][6][7]. Patients with pre-LT CKD suffer increased intraoperative blood loss and haemostatic abnormalities, bearing a 15% increased risk of post-operative mortality [8,9]. Common contributing factors of pre-LT CKD include haemodynamic instability, viral or bacterial infection and excessive use of nephrotoxic drugs, which may lead to prolonged ischaemic or toxic insults to the kidney [9][10][11][12].…”