Background: Disparity in chronic kidney disease progression among Black participants persists in glomerular diseases. Genetic variants in the Apolipoprotein L1 (APOL1) gene in the Black population contribute to kidney disease, but the influence in membranous nephropathy remains unknown. Methods: Longitudinally followed participants enrolled in the Glomerular Disease Collaborative Network (GDCN) or Cure Glomerulonephropathy Network (CureGN) were included if they had DNA or genotyping available for APOL1 (Black participants with membranous nephropathy) or had membranous nephropathy (non-Black participants). eGFR slopes were estimated using linear mixed effects models with random effects and adjusting for covariates and interactions terms of covariate. Fisher’s exact, Kruskal-Wallis test and Kaplan-Meier curves with log rank tests were used to compare group’s difference. Results: Among 118 Black membranous nephropathy participants, 16 (14%) had high-risk APOL1 genotype (2 risk alleles), and 102 (86%) had low-risk APOL1 genotype (0 or 1 risk alleles, n= 53 and n = 49, respectively). High-risk APOL1 membranous nephropathy participants were notably younger at disease onset than low-risk APOL1 and non-Black membranous nephropathy participants (n=572). eGFR at disease onset was not different between groups, though eGFR decline (slope) was steeper in participants with high-risk APOL1 genotype (-16± 2 (±SE) mL/min/1.73m2/year) compared to low-risk APOL1 genotype (-4± 0.8 mL/min/1.73m2/year) and non-Black membranous nephropathy participants (-2.0 ± 0.4 mL/min/1.73m2/year), p<0.0001). Time to kidney failure was faster in the high-risk APOL1 genotype than low-risk APOL1 genotype or non-Black membranous nephropathy participants. Conclusion: The prevalence of high-risk APOL1 variant among Black membranous nephropathy participants is comparable to the general Black population yet the high-risk genotype conferred worse eGFR decline and faster time to kidney failure compared to low-risk genotype and non-Black participants.