Abstract
KEY POINTS: Impaired early graft function effects differ by donor type: living donors show increased rejection/graft failure and deceased donors show mortality risk. Despite high-risk incompatible transplants, living donor recipients have low impaired graft function rates (4.5% versus 24.7% in deceased donors). Slow graft function is a distinct phenotype requiring recognition beyond traditional delayed graft function classification, with donor-specific implications. BACKGROUND: With the rise of high-risk living donor kidney transplantation, the effect of early graft function (EGF) on transplant outcomes remains unclear. METHODS: In this retrospective multicenter study, we classified kidney transplantation recipients (KTRs) based on EGF and donor type. EGF within the first post-transplant week was classified as immediate graft function, slow graft function (SGF), or delayed graft function (DGF), with impaired EGF defined as SGF or DGF. The primary outcomes included biopsy-proven acute rejection (BPAR) within 1 year, death-censored graft failure (DCGF), and overall mortality. RESULTS: Among 3261 KTRs, 365 (11.2%) experienced impaired EGF, including 190 (5.8%) with SGF and 175 (5.4%) with DGF. In living donor KTRs, impaired EGF was significantly associated with an increased risk of 1-year BPAR (adjusted hazard ratio [aHR], 2.13; 95% confidence interval [CI], 1.33 to 3.39) and DCGF (aHR, 2.49; 95% CI, 1.29 to 4.82) but not mortality. Both SGF and DGF increased the risk of BPAR, while only DGF significantly elevated the risk of DCGF. In deceased donor KTRs, impaired EGF was associated with a higher risk of both DCGF (aHR, 2.18; 95% CI, 1.43 to 3.31) and mortality (aHR, 2.30; 95% CI, 1.52 to 3.49) with SGF and DGF demonstrating similar patterns. Notably, prolonged DGF (≥7 days) was linked to progressively worse outcomes. CONCLUSIONS: The effect of impaired EGF varies by donor type. In living donor KTRs, impaired EGF increased the risks of BPAR and DCGF, particularly in cases of DGF. In deceased donor KTRs, impaired EGF elevated the risks of DCGF and mortality but not BPAR, highlighting the need for tailored strategies to optimize EGF.