Two coding variants of APOL1 account for much of the excess risk of focal segmental glomerulosclerosis in people of recent West African ancestry. There is an unmet need of treatment for apolipoprotein L1 kidney disease. In this issue, Sula Karreci et al. reported that lisinopril reduced proteinuria and glomerulosclerosis in a mouse model of apolipoprotein L1–induced focal segmental glomerulosclerosis, in a genotype-specific manner. By contrast, hydralazine and dapagliflozin had no effect. This study highlights the potential therapeutic utility of angiotensin-converting enzyme inhibitor in apolipoprotein L1 kidney disease.
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