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Comparison of Postdonation Kidney Function Between Caucasian Donors and Low-risk APOL1 Genotype Living Kidney Donors of African Ancestry

Gaillard, François, MD1,2; Gribouval, Olivier, PhD3; Courbebaisse, Marie, MD, PhD2,4,5; Fournier, Catherine, MSc1; Antignac, Corinne, MD, PhD3,6; Legendre, Christophe, MD1,2; Servais, Aude, MD, PhD1,2,3

doi: 10.1097/TP.0000000000002405
In Brief

1 Nephrology and Renal Transplantation Department, Necker Hospital, AP-HP, Paris, France.

2 Paris Descartes University, Sorbonne Paris Cité, France.

3 INSERM U1163, Institut Imagine, University Paris Descartes, Paris.

4 HôpitalEuropéen Georges Pompidou, Physiology Department, AP-HP, Paris, France.

5 INSERM, U1151, Paris, France.

6 Genetic Department, Necker Hospital, APHP, Paris, France.

Received 26 June 2018. Revision received 26 July 2018.

Accepted 29 July 2018.

The research leading to these results has received funding from the Investments for the Future Program grant ANR-10-IAHY-01 (to C.A.).

The authors declare no conflicts of interest.

F.G., A.S., C.L., and C.F. participated in research design. F.G., A.S., C.L., C.A., and M.C. participated in the writing of the article. F.G., A.S., O.G., and C.A. participated in the performance of the research. F.G., A.S., C.A., C.L., M.C.

Correspondence: François Gaillard, Nephrology and Transplantation Department, Hôpital Necker-Enfants Malades, 149 rue de Sèvres 75015, Paris, France. (gaillard.f@protonmail.com); Aude Servais, MD, PhD, Nephrology and Transplantation Department, Hôpital Necker, 149 rue de Sèvres, 75015 Paris, France. (aude.servais@aphp.fr).

ApolipoproteinL1 variants account for some of the increased risk of end-stage renal disease among living kidney donors of African descent,1,2 but may not summarize the totality of end-stage renal disease risk increase. We wondered whether early postdonation glomerular filtration rate (GFR) was different between donors of African ancestry with low-risk apolipoprotein L1 gene (APOL1) genotype and Caucasian donors. We compared compensatory response of the remaining kidney 1 year after donation between living kidney donors of Caucasian and African origin (16 from West Indies; 15 from West Africa), in a monocentric retrospective study at Necker hospital between January 2009 and December 2016, approved by the ethical committee.

We matched 62 Caucasian living kidney donors with 31 donors of African descent with low-risk APOL1 genotype (0 or 1 G1 or G2 allele of APOL1) on age, body mass index, measured GFR (mGFR), and sex. GFR was measured at baseline by 51-chromium ethylene diamnine tetra acetic acid urinary clearance. African and Caucasian donors had similar baseline mGFR (99.4 ± 11.3 mL/min per 1.73 m2 vs 97.4 ± 11.8 mL/min per 1.73 m2; P = 0.43), similar baseline estimated GFR (eGFR) (98.0 ± 16.0 mL/min per 1.73 m2 vs 96.3 ± 14.4 mL/min per 1.73 m2; P = 0.68), and similar 1-year postdonation eGFR (62.4 ± 12.9 mL/min per 1.73 m2 vs 65.6 ± 15.1 mL/min per 1.73 m2; P = 0.30). Baseline albumin-to-creatinine ratio and blood pressure were not different between groups. African donors had lower absolute eGFR increase after donation compared with white donors (+13.2 ± 10.9 mL/min per 1.73 m2 vs +18.1 ± 11.2 mL/min per 1.73 m2; P = 0.03). Relative eGFR increase after donation tended to be lower for donors of African ancestry compared to Caucasian donors (+29 ± 24% vs +39 ± 23%; P = 0.05). We previously reported that absolute eGFR increase after donation was negatively correlated with the baseline ratio of mGFR divided by the volume of the remaining kidney (mGFR/volume).3 Because absolute eGFR increase was different between groups, we compared renal volume and mGFR/volume. At baseline, African donors had lower remaining-kidney volume compared with white donors (122.4 ± 20.1 mL/1.73 m2 vs 127.9 ± 19.7 mL/1.73 m2; P = 0.04). Remaining kidney “mGFR/volume” ratio was higher in donors of African descent compared with white donors (0.42 ± 0.10 mL/min per mL vs 0.38 ± 0.07 mL/min per mL; P = 0.03).

Living kidney donors of African ancestry with low-risk APOL1 genotype have lower postdonation eGFR increase. The number of participants in each group limited the statistical power to detect eGFR differences at baseline and 1 year. Difference between baseline and 1 year reflects the slope of eGFR evolution after donation. A longer follow-up might reveal a statistically significant difference of postdonation eGFR between groups. For donors of African ancestry, lower kidney volume could reflect reduced nephron number.4 Because baseline mGFR is similar in both groups, reduced nephron number in African donors could reflect higher baseline single nephron GFR (snGFR). The “already high” snGFR in donors of African ancestry could limit postdonation GFR increase. In agreement, donors of African descent had lower postdonation eGFR increase. Nephron-number difference between groups could be linked to a lower birth weight of newborns of African ancestry as observed in African American.5

Our results suggest that even low-risk APOL1 donors have lower compensatory response compared with Caucasian donors. Therefore, APOL1 genotype may not be sufficient to explain the discrepancy between donors of African descent and white donors. Better description of living kidney donation outcomes of donors with low-risk APOL1 genotype is urgently needed.

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