106.[20221204]Deceased-Donor AKI and Acute Rejection in Kidney Transpl…
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Multicenter Study Am J Kidney Dis
. 2023 Feb;81(2):222-231.e1. doi: 10.1053/j.ajkd.2022.08.011. Epub 2022 Oct 1.
Deceased-Donor Acute Kidney Injury and Acute Rejection in Kidney Transplant Recipients: A Multicenter Cohort
Peter P Reese 1, Mona D Doshi 2, Isaac E Hall 3, Behdad Besharatian 4, Jonathan S Bromberg 5, Heather Thiessen-Philbrook 6, Yaqi Jia 6, Malek Kamoun 7, Sherry G Mansour 8, Enver Akalin 9, Meera N Harhay 10, Sumit Mohan 11, Thangamani Muthukumar 12, Bernd Schröppel 13, Pooja Singh 14, Francis L Weng 15, Chirag R Parikh 16
Affiliations expand
PMID: 36191727 PMCID: PMC9868058 (available on 2024-02-01) DOI: 10.1053/j.ajkd.2022.08.011
Abstract
Rationale & objective: Donor acute kidney injury (AKI) activates innate immunity, enhances HLA expression in the kidney allograft, and provokes recipient alloimmune responses. We hypothesized that injury and inflammation that manifested in deceased-donor urine biomarkers would be associated with higher rates of biopsy-proven acute rejection (BPAR) and allograft failure after transplantation.
Study design: Prospective cohort.
Setting & participants: 862 deceased donors for 1,137 kidney recipients at 13 centers.
Exposures: We measured concentrations of interleukin 18 (IL-18), kidney injury molecule 1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) in deceased donor urine. We also used the Acute Kidney Injury Network (AKIN) criteria to assess donor clinical AKI.
Outcomes: The primary outcome was a composite of BPAR and graft failure (not from death). A secondary outcome was the composite of BPAR, graft failure, and/or de novo donor-specific antibody (DSA). Outcomes were ascertained in the first posttransplant year.
Analytical approach: Multivariable Fine-Gray models with death as a competing risk.
Results: Mean recipient age was 54 ± 13 (SD) years, and 82% received antithymocyte globulin. We found no significant associations between donor urinary IL-18, KIM-1, and NGAL and the primary outcome (subdistribution hazard ratio [HR] for highest vs 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], respectively). In secondary analyses, we detected no significant associations between clinically defined AKI and the primary outcome or between donor biomarkers and the composite outcome of BPAR, graft failure, and/or de novo DSA.
Limitations: BPAR was ascertained through for-cause biopsies, not surveillance biopsies.
Conclusions: In a large cohort of kidney recipients who almost all received induction with thymoglobulin, donor injury biomarkers were associated with neither graft failure and rejection nor a secondary outcome that included de novo DSA. These findings provide some reassurance that centers can successfully manage immunological complications using deceased-donor kidneys with AKI.
Keywords: Kidney transplantation; acute kidney injury (AKI); biomarkers; biopsy-proven acute rejection (BPAR); de novo DSA; deceased organ donation; donor-specific antibody (DSA); graft failure; inflammation; injury hypothesis; organ acceptance.
Multicenter Study Am J Kidney Dis
. 2023 Feb;81(2):222-231.e1. doi: 10.1053/j.ajkd.2022.08.011. Epub 2022 Oct 1.
Deceased-Donor Acute Kidney Injury and Acute Rejection in Kidney Transplant Recipients: A Multicenter Cohort
Peter P Reese 1, Mona D Doshi 2, Isaac E Hall 3, Behdad Besharatian 4, Jonathan S Bromberg 5, Heather Thiessen-Philbrook 6, Yaqi Jia 6, Malek Kamoun 7, Sherry G Mansour 8, Enver Akalin 9, Meera N Harhay 10, Sumit Mohan 11, Thangamani Muthukumar 12, Bernd Schröppel 13, Pooja Singh 14, Francis L Weng 15, Chirag R Parikh 16
Affiliations expand
PMID: 36191727 PMCID: PMC9868058 (available on 2024-02-01) DOI: 10.1053/j.ajkd.2022.08.011
Abstract
Rationale & objective: Donor acute kidney injury (AKI) activates innate immunity, enhances HLA expression in the kidney allograft, and provokes recipient alloimmune responses. We hypothesized that injury and inflammation that manifested in deceased-donor urine biomarkers would be associated with higher rates of biopsy-proven acute rejection (BPAR) and allograft failure after transplantation.
Study design: Prospective cohort.
Setting & participants: 862 deceased donors for 1,137 kidney recipients at 13 centers.
Exposures: We measured concentrations of interleukin 18 (IL-18), kidney injury molecule 1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) in deceased donor urine. We also used the Acute Kidney Injury Network (AKIN) criteria to assess donor clinical AKI.
Outcomes: The primary outcome was a composite of BPAR and graft failure (not from death). A secondary outcome was the composite of BPAR, graft failure, and/or de novo donor-specific antibody (DSA). Outcomes were ascertained in the first posttransplant year.
Analytical approach: Multivariable Fine-Gray models with death as a competing risk.
Results: Mean recipient age was 54 ± 13 (SD) years, and 82% received antithymocyte globulin. We found no significant associations between donor urinary IL-18, KIM-1, and NGAL and the primary outcome (subdistribution hazard ratio [HR] for highest vs 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], respectively). In secondary analyses, we detected no significant associations between clinically defined AKI and the primary outcome or between donor biomarkers and the composite outcome of BPAR, graft failure, and/or de novo DSA.
Limitations: BPAR was ascertained through for-cause biopsies, not surveillance biopsies.
Conclusions: In a large cohort of kidney recipients who almost all received induction with thymoglobulin, donor injury biomarkers were associated with neither graft failure and rejection nor a secondary outcome that included de novo DSA. These findings provide some reassurance that centers can successfully manage immunological complications using deceased-donor kidneys with AKI.
Keywords: Kidney transplantation; acute kidney injury (AKI); biomarkers; biopsy-proven acute rejection (BPAR); de novo DSA; deceased organ donation; donor-specific antibody (DSA); graft failure; inflammation; injury hypothesis; organ acceptance.
