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Background  Hypertension (HTN) disproportionately affects African Americans (AAs), who respond better to thiazide diuretics than other antihypertensives. Variants of the  APOL1  gene found in AAs are associated with a higher rate of kidney disease and play a complex role in cardiovascular disease.    Methods  AA subjects from four HTN trials (n = 961) (GERA1, GERA2, PEAR1, and PEAR2) were evaluated for blood pressure (BP) response based on  APOL1  genotype after 4–9 weeks of monotherapy with thiazides, beta blockers, or candesartan.  APOL1  G1 and G2 variants were determined by direct sequencing or imputation.    Results  Baseline systolic BP (SBP) and diastolic BP (DBP) levels did not differ based on  APOL1  genotype. Subjects with 1–2  APOL1  risk alleles had a greater SBP response to candesartan (-12.2 +/- 1.2 vs -7.5 +/- 1.8 mmHg,  p  = 0.03; GERA2), and a greater decline in albuminuria with candesartan (-8.3 +/- 3.1 vs +3.7 +/- 4.3 mg/day,  p  = 0.02).  APOL1  genotype did not associate with BP response to thiazides or beta blockers. GWAS was performed to determine associations with BP response to candesartan depending on  APOL1  genotype. While no SNPs reached genome wide significance, SNP rs10113352, intronic in  CSMD1 , predicted greater office SBP response to candesartan ( p  = 3.7 x 10 −7 ) in those with 1–2 risk alleles, while SNP rs286856, intronic in  DPP6 , predicted greater office SBP response ( p  = 3.2 x 10 −7 ) in those with 0 risk alleles.    Conclusions  Hypertensive AAs without overt kidney disease who carry 1 or more  APOL1  risk variants have a greater BP and albuminuria reduction in response to candesartan therapy. BP response to thiazides or beta blockers did not differ by  APOL1  genotype. Future studies confirming this initial finding in an independent cohort are required.

Hypertensive APOL1 risk allele carriers demonstrate greater blood pressure reduction with angiotensin receptor blockade compared to low risk carriers