TY - JOUR
T1 - Blood pressure and APOL1 risk variants in a South African chronic haemodialysis population of African ancestry
AU - van Hougenhouck-Tulleken, Wesley
AU - Rheeder, Paul
AU - van Rensburg, Elizabeth J.
N1 - Publisher Copyright:
© The Author(s) 2026. Published by Oxford University Press on behalf of the ERA. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site-for further information please contact [email protected]
PY - 2026/9
Y1 - 2026/9
N2 - 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 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. By 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% confidence interval (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.
AB - 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 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. By 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% confidence interval (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.
KW - APOL1
KW - African ancestry
KW - blood pressure
KW - chronic kidney disease
KW - haemodialysis
UR - https://www.scopus.com/pages/publications/105050524389
U2 - 10.1093/ckj/sfag295
DO - 10.1093/ckj/sfag295
M3 - Article
C2 - 42761223
AN - SCOPUS:105050524389
SN - 2048-8505
VL - 19
JO - Clinical Kidney Journal
JF - Clinical Kidney Journal
IS - 9
M1 - sfag295
ER -