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OC-063 The severity of hepatic ischaemia-reperfusion injury is associated with acute kidney injury following donation after brain death liver transplantation
  1. J A Leithead1,2,
  2. M J Armstrong1,2,
  3. C Corbett1,2,
  4. M Andrew1,
  5. C Kothari1,
  6. B K Gunson2,
  7. P Muiesan1,
  8. J W Ferguson1
  1. 1Liver Unit, Queen Elizabeth Hospital, UK
  2. 2NIHR Biomedical Research Unit and Centre for Liver Research, University of Birmingham, Birmingham, UK

Abstract

Introduction Donation after Cardiac Death liver transplant recipients have an increased frequency of acute kidney injury (AKI) during the immediate post-operative period and in these patients peak peri-operative aspartate amino-transferase (AST), a surrogate marker of hepatic ischaemia-reperfusion injury (IRI), is the only variable associated with renal dysfunction (Leithead et al Am J Transplant 2012). This suggests that hepatic IRI may play a critical role in the pathogenesis of AKI after liver transplantation. The aim of this study was to determine if graft injury is also associated with renal dysfunction following Donation after Brain Death (DBD) liver transplantation.

Methods Single-centre study of 290 patients who underwent first whole DBD liver transplantation for chronic liver disease 01/2007–06/2011. Peak peri-operative serum AST was recorded as a marker of hepatic IRI. AKI was defined according to the RIFLE criteria: peak serum creatinine ≥2 times baseline.

Results The median peak peri-operative AST was 1307 U/l. Peak AST correlated well with the histological grading of IRI on “time zero” allograft biopsy (p=0.007). The median peak peri-operative creatinine was 125 (IQR 91–191) μmol/l. The median percentage change in creatinine from baseline was +49 (IQR 12–119). 36.9% of patients developed AKI, of whom 58.9% required renal replacement therapy. Patient survival was reduced in the AKI group (AKI, 82.8%; no AKI, 95.5%, estimated 1-year survival; log rank p=0.001). On univariate analysis peak AST correlated with both peak creatinine (r=0.259, p<0.001) and peak change in creatinine from baseline (r=0.309, p<0.001). Median peak AST was higher in AKI patients (1755 vs 1158 U/l; p<0.001). The incidence of AKI was 25.7%, 41.0% and 75.0% for patients with a peak AST of <1500, 1500–3000 and ≥3000 U/l, respectively (p<0.001). On multiple logistic regression analysis the variables associated with AKI were black ethnicity (p=0.043), pre-transplant MELD (p=0.047), pre-transplant refractory ascites (p=0.047), intra-operative red cell concentrate requirements (p<0.001), peri-operative sepsis (p<0.001) and peak peri-operative AST (p<0.001).

Conclusion Hepatic IRI demonstrates a strong relationship with peri-operative AKI in DBD liver transplant recipients. Hepatic IRI may therefore play an important and modifiable role in the pathogenesis of renal dysfunction in this setting.

Competing interests None declared.

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