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Clinically Adjudicated Deceased Donor Acute Kidney Injury and Graft Outcomes

Sherry G. Mansour, Nadeen Khoury, Ravi Kodali, Sarthak Virmani, Peter P. Reese, Isaac E. Hall, Yaqi Jia, Yu Yamamoto, Heather R. Thiessen-Philbrook, Wassim Obeid, Mona D. Doshi, Enver Akalin, Jonathan S. Bromberg, Meera N. Harhay, Sumit Mohan, Thangamani Muthukumar, Pooja Singh, Francis L. Weng, Dennis G. Moledina, Jason H. Greenberg, Francis P. Wilson, Chirag R. Parikh

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.

Less than 20% of patients on the waiting list receive kidney transplants each year, and approximately thirteen patients die every day awaiting a kidney transplant. Despite this unmet demand, 20% of deceased-donor kidneys are discarded, with kidneys from donors with acute kidney injury (AKI) being procured at lower rates and discarded at higher rates. Donor AKI usually occurs in the setting of brain-death and significant hemodynamic changes.


Study design
This was an ancillary study from the Deceased Donor Study (DDS) and included 428 deceased donors with available charts from two organ procurement organizations (OPOs); Gift of Life Michigan and New York Organ Donor Network. Overall DDS methods have been described in detail elsewhere [14,15]. For the current study, a trained research coordinator manually abstracted seven demographic variables and 50 longitudinal variables from charts of donor hospitalizations from April 2010 to November 2013.

Biomarker measurement
After collection at time of organ procurement, urine samples were centrifuged at 1000×g for 10 minutes at 4°C, separated into 1 ml aliquots, and immediately stored at -80°C until biomarker measurement.

We evaluated associations between clinically adjudicated deceased-donor AKI and recipient outcomes in this multicenter study. We found that clinically phenotyped deceased-donor AKI had biological differences as evidenced by urine injury and repair biomarkers. We also found that donor iAKI happening earlier during donor hospitalization or ongoing at organ procurement was significantly associated with increased risk of DGF and lower 1-year eGFR but was not associated with early GF.

We would like to thank all the families of the deceased donors and all the recipients who allowed for this science to progress. We are eternally indebted to your contributions to the field of kidney transplant.

The data reported here have been supplied by the United Network for Organ Sharing (UNOS) as the contractor for the OPTN. The interpretation and reporting of these data are the responsibility of the author(s) and in no way should be seen as an official policy of or interpretation by the OPTN or the U.S. Government.

The content is the responsibility of the authors alone and does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. These organizations were not involved in study design, analysis, interpretation, or manuscript creation.

Citation: Mansour SG, Khoury N, Kodali R, Virmani S, Reese PP, Hall IE, et al. (2022) Clinically adjudicated deceased donor acute kidney injury and graft outcomes. PLoS ONE 17(3): e0264329.

Editor: Stanislaw Stepkowski, University of Toledo, UNITED STATES

Received: June 11, 2021; Accepted: February 8, 2022; Published: March 3, 2022.

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.

Data Availability: All relevant data are within the manuscript and its Supporting Information files.

Funding: This statement reflects the correct funding associated with this work: This work was supported by the American Heart Association grant 18CDA34110151 and the Patterson Trust Fund to Dr. Mansour; National Institutes of Health (NIH)/National Institutes of Diabetes and Digestive and Kidney Diseases (NIDDK) grant R01DK-93770, grant K24DK090203 to Dr. Parikh. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

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