This study clearly depicts that It is well recognized that African Americans of sub-Saharan African ancestry have nearly a 4-fold increased prevalence of endstage kidney disease (ESKD) over European Americans1,2,3,4. In 2008, two coding alleles in the apolipoprotein L1 gene (APOL1), G1 and G2, were discovered to account for the majority of excess risk in progressive nondiabetic kidney disease in African Americans1,2,3,5. The several forms of APOL-1–associated kidney disease include focal segmental glomerulosclerosis (FSGS), human immunodeficiency virus–associated nephropathy (HIVAN), hypertension-attributed ESKD, and sickle cell nephropathy5,6,7,8. There is a strong biallelic effect observed such that a high-risk genotype defined as the presence of 2 APOL1 risk alleles confers the strongest risk for HIVAN in the United States7 with an OR of 29 (95% CI 13–68), and an OR of 89 (95% CI 18–912) in South Africa9. This observation of stronger adverse kidney outcomes associated with APOL1 risk alleles was the rationale for a report by Vajgel, et al10 that appears in this issue of The Journal.

Their study involved genotyping APOL1 G1 and G2 risk alleles in 201 nonwhite Brazilian patients with lupus nephritis (LN) and 222 healthy blood donors. Because of the low APOL1 biallelic frequency in LN cases (2%), the authors had limited power to test biallelic effects and instead examined monoallelic APOL1 risk allele effect on LN outcomes.

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