Influence of donor warm ischemia time on development of acute kidney injury after DCD liver transplantation

M. Kalisvaart, J.E. de Haan, D.A. Hesselink, W.G. Polak, B.E. Hansen, J.N.M Ijzermans, H.J. Metselaar, J. de Jonge

Chair(s): dr. Robert A. Pol, vaat-en transplantatiechirurg, UMC Groningen & dr. Wojaiech G. Polak, chirurg, Erasmus MC

Thursday 10 march 2016

9:20 - 9:30h at Zaal 5 & 6

Categories: Parallelsessie (klinisch)

Parallel session: Parallelsessie VIII - Klinisch chirurgisch en acuut

Acute kidney injury (AKI) after liver transplantation (LT) is observed in over 50% of the donation after circulatory death (DCD) recipients. This phenomenon has been attributed to the additional donor warm ischemia time (DWIT) with subsequent increase of hepatic ischemia/reperfusion injury (IRI). As of today, various definitions of DWIT are used and little is known about its influence on the development of postoperative AKI. Our objective was to analyze the impact of DWIT on development and severity AKI after DCD LT.

Development of AKI, according to AKIN criteria, after DCD LT in our hospital was retrospectively assessed from July 2008 until April 2015. DWIT was divided into two periods: donor agonal phase (time from saturation <80% or MAP <50 mmHg to asystole) and absolute DWIT (time from asystole to start of cold perfusion). A multivariable logistic regression model (using backward likelihood estimation) with all clinical relevant donor, recipient, and intraoperative factors was created to identify factors associated with development of AKI. Postoperative peak serum aspartate aminotransferase (AST) was used as a surrogate marker for hepatic IRI.

Seventy DCD recipients were included of whom 40 (57%) developed AKI. Agonal phase was longer in the AKI group (15 vs. 11 min; p=0.020). Surprisingly, absolute DWIT was shorter in the AKI group (15 vs. 18 min; p=0.050). Mean donor agonal phase however, correlated well with severity of AKI (no AKI, 11 min; AKIN 1, 13 min; AKIN 2, 16 min; AKIN 3, 20 min; p=0.014). This correlation was not observed for the mean absolute DWIT (no AKI, 18 min; AKIN 1, 16 min; AKIN 2, 16 min; AKIN 3, 17 min; p=0.205). The multivariable logistic regression model identified donor agonal phase as an independent factor associated with AKI (OR 1.104; 95% CI 1.014-1.203; p=0.023). Also peak serum AST increased with length of donor agonal phase (p=0.002), but was not congruent with absolute DWIT (p=0.374).

Our results suggest that not absolute DWIT, but length of donor agonal phase has an important influence on development and severity of AKI after DCD LT. Moreover, the severity of hepatic IRI also increases with length of donor agonal phase. This study provides new insight on the importance of the agonal phase on the severity of AKI and hepatic IRI after DCD liver transplantation.