The following is a summary of “Deceased-Donor Acute Kidney Injury and Acute Rejection in Kidney Transplant Recipients: A Multicenter Cohort,” published in the February 2023 issue of the Kidney Diseases by Reese et al.
Donor acute kidney injury (AKI) increases innate immunity, upregulates HLA expression in the kidney allograft, and elicits alloimmune responses in the recipient. Researchers expected that greater rates of biopsy-proven acute rejection (BPAR) and allograft failure following transplantation would be related to damage and inflammation indicators in the urine of deceased donors. Interleukin 18 (IL-18), kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin (NGAL) concentrations were determined in the urine of dead donors.
Donor clinical AKI was evaluated using their criteria and those established by the Acute Kidney Injury Network (AKIN). The primary outcome was a combined measure of BPAR and graft failure unrelated to mortality. The combination of donor-specific antibody (DSA), graft failure, and BPAR was considered a secondary outcome. Results were evaluated one year after the transplant. The average age of those who got antithymocyte globulin was 54 years (standard deviation, 13 years).
Subdistribution HR for highest versus lowest tertile of 0.76 [95% CI, 0.45-1.28], 1.20 [95% CI, 0.69-2.07], and 1.14 [95% CI, 0.71-1.84] for donor urinary IL-18, KIM-1, and NGAL, respectively, did not show any significant relationships with the primary outcome. Clinically defined AKI and the primary result were not significantly associated in additional analyses, nor were donor biomarkers and the composite outcome of BPAR, graft failure, and/or de novo DSA. Donor damage biomarkers were unrelated to graft failure and rejection or a secondary outcome that included de novo DSA in a large cohort of kidney recipients who almost all had an induction with thymoglobulin. These results give centers using kidneys from dead donors some comfort in dealing with immunological problems.
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