Blood pressure and APOL1 risk variants in a South African chronic haemodialysis population of African ancestry

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Abstract Background APOL1 risk variants are strongly associated with kidney disease in individuals of recent African ancestry, but their haemodynamic effects remain incompletely characterised, particularly in African dialysis populations. We evaluated the association between APOL1 variants and blood pressure phenotypes in a South African haemodialysis cohort. Methods In this cross-sectional study, 115 adults receiving maintenance haemodialysis in Pretoria were included. All participants were self-identified Black Africans. APOL1 genotyping (G1: rs73885319, rs60910145; G2: rs71785313) was performed, and genetic models were analysed as additive, dominant, and recessive. Pre-dialysis blood pressure was defined as the mean of five consecutive measurements. Outcomes included systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP). Associations were assessed using linear mixed-effects models with dialysis site as a random effect, with sequential adjustment for age, sex, and antihypertensive class burden. Results APOL1 risk allele distribution was 53.0% zero, 36.5% one, and 10.4% two alleles. There were no consistent associations between APOL1 genotype and SBP, DBP, or MAP in univariate analyses. In multivariable models, SBP was significantly lower in APOL1 risk allele carriers under additive and dominant models. In contrast, PP was consistently lower in APOL1 risk allele carriers and remained significant after full adjustment (additive model, one vs zero: β -7.772, 95% CI -13.009 to -2.535, P = 0.004; dominant model: β -7.69 95% CI -12.622 to -2.757, P = 0.003). No consistent associations were observed for DBP or MAP. Conclusions In this cohort of Black African haemodialysis patients, APOL1 risk variants were associated with lower PP and, after adjustment, lower SBP, without differences in DBP or MAP. These findings suggest a distinct haemodynamic phenotype characterised by reduced arterial pulsatility and highlight the need for further mechanistic and prospective studies, particularly in the context of emerging APOL1-targeted therapies.

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