Genetic Risk of Primary Aldosteronism and Its Contribution to Hypertension: A Cross-Ancestry Meta-Analysis of Genome-Wide Association Studies
Pooled result · Genome-wide significant loci for PA (meta-analysis)Result — go to the resultOdds ratio 1.50 95% CI 1.33–1.69Authors' conclusion
This study demonstrates the genome-wide evidence for a genetic predisposition to PA susceptibility in the cross-ancestry cohorts and its significant contribution to the genetic background of hypertension.
Study context
- Population
- Japanese, UK Biobank and FinnGen cohorts
- Participants
- 816 vs 425,239
- Comparison
- Primary aldosteronism (PA) cases vs controls
- PA casesn = 816
- Controlsn = 425,239reference
- Outcome
- Genetic variants contributing to PA susceptibility
Methodological detailsJapanese GWAS combined with UK Biobank and FinnGen cohorts
- Japanese GWAS combined with UK Biobank and FinnGen cohorts
Pooled result
As reported in the abstract
Genome-wide significant loci for PA (meta-analysis)
Odds ratio
1.50
95% CI 1.33–1.69
P = 5.2×10-11
PA cases vs controls
OR 1.50 (95% CI 1.33–1.69); P = 5.2×10-11
- Genome-wide significant loci (1p13, 7p15, 11p15, 12q24, 13q12; P<5.0×10-8)
- 5
Further pooled results
Loci with suggestive association, Japanese GWAS (P<1.0×10-6)
- Suggestive loci
- 10
8q24 (CYP11B2) gene-based test
- Nearly genome-wide significant locus; significant in gene-based test
- P = 7.2×10-7
Previously established BP-associated variants: higher risk effect for PA than hypertension
- Proportion of 42 BP variants with higher risk effect for PA
- 66.7%
Original publication
Genetic Risk of Primary Aldosteronism and Its Contribution to Hypertension: A Cross-Ancestry Meta-Analysis of Genome-Wide Association Studies. Circulation. Published 21 February 2023. doi:10.
Summarised from the published abstract; every number is checked against it