Introduction: Increasing evidence suggests an independent association of hepatic steatosis with chronic kidney disease, kidney function decline and risk of cardiovascular (CV) disease. Whether the presence or severity of an organ donor’s hepatic steatosis impacts on kidney transplant recipient (KTR) outcomes has not been studied.

Methods: We performed a retrospective cohort study of deceased liver donors, matched to their KTR, in New South Wales (NSW), Australia from 2006-2020. We linked data from the Australian and New Zealand Dialysis and Transplantation (ANZDATA) and Organ Donation (ANZOD) registries with biopsy results of donor livers evaluated or utilised for transplantation at the NSW state-wide liver transplant unit. Donor hepatic steatosis was graded contemporaneously by histopathologists as S0 (<5%), S1 (5-33%), S2 (>33-66%) or S3 (>66%). Standard donor and recipient characteristics were collected. All-cause death, cardiovascular (CV) death, graft loss (death-censored), delayed graft function (DGF), graft function decline (assessed by eGFR) and post-transplant CV events (composite of coronary artery, peripheral vascular or cerebrovascular disease) were compared among recipients according to their presence and severity of hepatic steatosis.

Results: 751 donors with liver biopsies were matched to 1,263 KTRs (8,043 person-years follow-up). Donor hepatic steatosis grades were: S0 453 (60%), S1 195 (26%), S2 71 (9%), S3 32 (4%). Donors with hepatic steatosis (S1-3) were significantly older (median age 53 vs 46 years) than those without steatosis and had worse metabolic profiles: higher body mass index (median 27 vs 25kg/m2), diabetes (9% vs 6%), hypertension (35% vs 25%). KTR of donors with and without hepatic steatosis had similar baseline characteristics. Presence of hepatic steatosis (vs no steatosis) and steatosis severity (S3 vs S0-2) did not impact on all-cause- or CV-death, graft loss, or DGF in the multivariable analysis. Univariable analysis suggested that decline in graft function was greater in recipients from donors with steatosis compared to recipients of donors without steatosis, but this no longer remained significant on multivariable analysis after adjusting for other variables. There was an increased risk of CV events on univariable (HR 1.42, 95%CI 1.00-2.02, p=0.05) and multivariable analysis (HR 1.47, 95%CI 1.03-2.10, p=0.04, Table 1) among recipients of donors with severe (S3) steatosis versus those with no/less donor steatosis.

Conclusion: In this retrospective analysis, neither the presence nor severity of biopsy-proven donor hepatic steatosis appeared to impact kidney transplant recipient outcomes. Recipients from donors with severe hepatic steatosis may be at higher risk of cardiovascular events.