Abstract Background and aims Acute kidney injury (AKI) occurs in up to 60% of liver transplant recipients and is associated with increased morbidity and mortality. Graft steatosis has emerged as a risk factor for post-transplant AKI (LTx-AKI), attributed to increased susceptibility to ischaemia–reperfusion injury (IRI). We hypothesised that steatotic livers drive AKI independently of IRI, through the release of toxic lipids into the circulation. This study evaluated whether donor liver steatosis is associated with LTx-AKI in a large, multi-center database (NHBST), and whether this association persists after accounting for increased IRI risk. Methods We conducted a retrospective cohort study of 18 189 adult liver transplant recipients from the NHSBT registry (1980–2025). Donor steatosis was identified at procurement. The primary outcome was AKI. Multivariable logistic regression assessed the association between steatosis and AKI, adjusting for donor, recipient and intraoperative factors. Results Donor steatosis was associated with higher risk of AKI (OR 1.27, 95% c.i. 1.15–1.41, P 0.0001) after full adjustment. Donor risk index (DRI) was used as a proxy for risk of hepatic IRI. Interaction terms between steatosis and DRI were non-significant (P 0.1), indicating an effect independent of IRI. Subgroup analyses confirmed consistent association between donor steatosis and LTx-AKI in both low (≤1.35; OR 1.31, 95% c.i. 1.07–1.61) and high (≥1.7; OR 1.26, 95% c.i. 1.05–1.51) DRI groups. Conclusions Donor liver steatosis independently predicts post-transplant AKI. These findings support a direct lipotoxic effect, whereby lipid release from steatotic grafts at reperfusion potentially contributes to renal injury.
Otunla et al. (Sun,) studied this question.