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Author Notes:

Correspondence: Barry I. Freedman, MD, Department of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1053. (bfreedma@wakehealth.edu);

Jasmin Divers, PhD, Division of Public Health Sciences, Department of Biostatistical Sciences, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157. (jdivers@wakehealth.edu).

The data reported here have been supplied by the Minneapolis Medical Research Foundation (MMRF) as the contractor for the Scientific Registry of Transplant Recipients (SRTR).

The interpretation and reporting of these data are the responsibilities of the authors and in no way should be considered as an official policy of or interpretation by the SRTR or the United States Government.

The authors declare no conflicts of interest.

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Research Funding:

This work was supported, in part, by NIH RO1 DK070941 (BIF), NIH RO1 DK084149 (BIF), NIH RO1 MD009055 (JD, BIF), and NIH/NIAD Genomics of Transplantation 5U19-AI070119 (AKI).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Surgery
  • Transplantation
  • NONDIABETIC NEPHROPATHY
  • ALLOGRAFT SURVIVAL
  • UNITED-STATES
  • ORGAN DONORS
  • GENE-GENE
  • RECIPIENTS
  • VARIANTS
  • ASSOCIATION
  • DISEASE
  • RISK

APOL1 Genotype and Kidney Transplantation Outcomes From Deceased African American Donors

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Journal Title:

Transplantation

Volume:

Volume 100, Number 1

Publisher:

, Pages 194-202

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Background. Two apolipoprotein L1 gene (APOL1) renal-risk variants in donors and African American (AA) recipient race are associated with worse allograft survival in deceased-donor kidney transplantation (DDKT) from AA donors. To detect other factors impacting allograft survival from deceased AA kidney donors, APOL1 renal-risk variants were genotyped in additional AA kidney donors. Methods. The APOL1 genotypes were linked to outcomes in 478 newly analyzed DDKTs in the Scientific Registry of Transplant Recipients. Multivariate analyses accounting for recipient age, sex, race, panel-reactive antibody level, HLAmatch, cold ischemia time, donor age, and expanded criteria donation were performed. These 478 transplantations and 675 DDKTs from a prior report were jointly analyzed. Results. Fully adjusted analyses limited to the new 478 DDKTs replicated shorter renal allograft survival in recipients of APOL1 2-renal-risk-variant kidneys (hazard ratio [HR], 2.00; P = 0.03). Combined analysis of 1153 DDKTs from AA donors revealed donor APOL1 high-risk genotype (HR, 2.05; P = 3 - 10-4), older donor age (HR, 1.18; P = 0.05), and younger recipient age (HR, 0.70; P = 0.001) adversely impacted allograft survival. Although prolonged allograft survival was seen in many recipients of APOL1 2-renal-risk-variant kidneys, follow-up serum creatinine concentrations were higher than that in recipients of 0/1 APOL1 renal-risk-variant kidneys. A competing risk analysis revealed that APOL1 impacted renal allograft survival, but not recipient survival. Interactions between donor age and APOL1 genotype on renal allograft survival were nonsignificant. Conclusions. Shorter renal allograft survival is reproducibly observed after DDKT from APOL1 2-renal-risk-variant donors. Younger recipient age and older donor age have independent adverse effects on renal allograft survival.

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©2015 Wolters Kluwer Health, Inc. All rights reserved.

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