TY - JOUR
T1 - Clinically adjudicated deceased donor acute kidney injury and graft outcomes
AU - Mansour, Sherry G.
AU - Khoury, Nadeen
AU - Kodali, Ravi
AU - Virmani, Sarthak
AU - Reese, Peter P.
AU - Hall, Isaac E.
AU - Jia, Yaqi
AU - Yamamoto, Yu
AU - Thiessen-Philbrook, Heather R.
AU - Obeid, Wassim
AU - Doshi, Mona D.
AU - Akalin, Enver
AU - Bromberg, Jonathan S.
AU - Harhay, Meera N.
AU - Mohan, Sumit
AU - Muthukumar, Thangamani
AU - Singh, Pooja
AU - Weng, Francis L.
AU - Moledina, Dennis G.
AU - Greenberg, Jason H.
AU - Wilson, Francis P.
AU - Parikh, Chirag R.
N1 - Publisher Copyright:
© 2022 Mansour et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2022/3
Y1 - 2022/3
N2 - Background Acute kidney injury (AKI) in deceased donors is not associated with graft failure (GF). We hypothesize that hemodynamic AKI (hAKI) comprises the majority of donor AKI and may explain this lack of association. Methods In this ancillary analysis of the Deceased Donor Study, 428 donors with available charts were selected to identify those with and without AKI. AKI cases were classified as hAKI, intrinsic (iAKI), or mixed (mAKI) based on majority adjudication by three nephrologists. We evaluated the associations between AKI phenotypes and delayed graft function (DGF), 1- year eGFR and GF. We also evaluated differences in urine biomarkers among AKI phenotypes. Results Of the 291 (68%) donors with AKI, 106 (36%) were adjudicated as hAKI, 84 (29%) as iAKI and 101 (35%) as mAKI. Of the 856 potential kidneys, 669 were transplanted with 32% developing DGF and 5% experiencing GF. Median 1-year eGFR was 53 (IQR: 41-70) ml/ min/1.73m2. Compared to non-AKI, donors with iAKI had higher odds DGF [aOR (95%CI); 4.83 (2.29, 10.22)] and had lower 1-year eGFR [adjusted B coefficient (95% CI): -11 (-19, -3) mL/min/1.73 m2]. hAKI and mAKI were not associated with DGF or 1-year eGFR. Rates of GF were not different among AKI phenotypes and non-AKI. Urine biomarkers such as NGAL, LFABP, MCP-1, YKL-40, cystatin-C and albumin were higher in iAKI. Conclusion iAKI was associated with higher DGF and lower 1-year eGFR but not with GF. Clinically phenotyped donor AKI is biologically different based on biomarkers and may help inform decisions regarding organ utilization.
AB - Background Acute kidney injury (AKI) in deceased donors is not associated with graft failure (GF). We hypothesize that hemodynamic AKI (hAKI) comprises the majority of donor AKI and may explain this lack of association. Methods In this ancillary analysis of the Deceased Donor Study, 428 donors with available charts were selected to identify those with and without AKI. AKI cases were classified as hAKI, intrinsic (iAKI), or mixed (mAKI) based on majority adjudication by three nephrologists. We evaluated the associations between AKI phenotypes and delayed graft function (DGF), 1- year eGFR and GF. We also evaluated differences in urine biomarkers among AKI phenotypes. Results Of the 291 (68%) donors with AKI, 106 (36%) were adjudicated as hAKI, 84 (29%) as iAKI and 101 (35%) as mAKI. Of the 856 potential kidneys, 669 were transplanted with 32% developing DGF and 5% experiencing GF. Median 1-year eGFR was 53 (IQR: 41-70) ml/ min/1.73m2. Compared to non-AKI, donors with iAKI had higher odds DGF [aOR (95%CI); 4.83 (2.29, 10.22)] and had lower 1-year eGFR [adjusted B coefficient (95% CI): -11 (-19, -3) mL/min/1.73 m2]. hAKI and mAKI were not associated with DGF or 1-year eGFR. Rates of GF were not different among AKI phenotypes and non-AKI. Urine biomarkers such as NGAL, LFABP, MCP-1, YKL-40, cystatin-C and albumin were higher in iAKI. Conclusion iAKI was associated with higher DGF and lower 1-year eGFR but not with GF. Clinically phenotyped donor AKI is biologically different based on biomarkers and may help inform decisions regarding organ utilization.
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U2 - 10.1371/journal.pone.0264329
DO - 10.1371/journal.pone.0264329
M3 - Article
C2 - 35239694
AN - SCOPUS:85125689221
SN - 1932-6203
VL - 17
JO - PLoS One
JF - PLoS One
IS - 3 March
M1 - e0264329
ER -