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Introduction: This study describes patient characteristics and examines graft function of kidney transplant recipients (without primary hyperoxaluria) with elevated plasma oxalate (POx) and enteric risk factors prior to transplant at our institution. Methods: Kidney transplant recipients between 2012 to 2020 with elevated POx at the time of kidney transplant evaluation were included. A matched control cohort was gathered using patient/donor age, living/deceased donor type, panel reactive antibody (PRA), kidney donor profile index (KDPI), and human leukocyte antigen (HLA) mismatch as matching variables. Graft function at 1 year and at last follow-up was reported. Results: A total of 106 patients with elevated POx were identified. A third of the patients had Roux-en-Y gastric bypass, a third had other enteric risks, and a third did not have an identifiable enteric risk. Median eGFR (estimated glomerular filtration rate) at 1-year and at last follow-up were similar between cases and controls except for subgroup of patients with pre-transplant POx >30mcmol/L where 1-year eGFR was lower compared to controls. Across eGFR categories, more cases were in eGFR category 30mcmol/L pre-transplant.

Ischemia-reperfusion (IR) injury plays a significant role in the pathogenesis of both delayed graft function (DGF) in allografts and hemodynamic mediated acute kidney injury (AKI) of native kidneys. IR injury involves the interplay of several factors, including both the innate and adaptive immune systems. Though the final effector mechanisms causing injury are likely similar in both allograft and native kidneys, DGF is confounded by various donor, recipient and graft-handling factors. DGF is becoming increasingly important because of the growing number of patients awaiting kidney transplant. Identifying mediators, new diagnostics and therapeutics for DGF is important to provide more kidneys for transplant and improve outcomes. Furthermore, given that DGF occurs in a tightly controlled scenario, studying DGF is useful for early studies of proof of principle for biomarkers and therapeutics prior to launching into less wellcontrolled studies in large numbers of native kidney AKI patients.