ArticleMedicine2025
Causal association between genetically predicted primary aldosteronism and aortic aneurysm and aortic dissection: A Mendelian randomization study.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Contained Rupture of the Ascending Aorta Caused by Primary Aldosteronism.Annals of thoracic surgery short reports · 2026Article
- High prevalence of primary aldosteronism and its impact on diabetic kidney disease in type 2 diabetes mellitus: A retrospective cohort study.Endocrine · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Emerging research indicates a potential pathogenic overlap between primary aldosteronism (PA) and aortic aneurysm (AA)/aortic dissection (AD). Despite case reports suggest a potential link between PA and AA/AD, the causality of this relationship remains unclear. This study is the first to elucidate the causal association between genetically predicted PA and the risk of AA and AD through Mendelian randomization (MR) analysis. Genome-wide significant single nucleotide polymorphisms associated with PA were identified from publicly available genome-wide association study summary statistics. Genetic associations with AA and AD were obtained from the FinnGen database. The inverse-variance weighted (IVW) method, along with complementary MR analysis methods, was employed to generate primary estimates. Sensitivity analyses were performed to ensure the robustness of findings. MR analyses utilizing the IVW method revealed a significant causal association between genetically predicted PA and the risk of AA (OR = 1.038; 95% CI = 1.024-1.053; P < .01), thoracic AA (OR = 1.066; 95% CI = 1.045-1.087; P < .01) and AD (OR = 1.165; 95% CI = 1.113-1.219; P < .01). Conversely, no significant association was observed between PA and abdominal AA (OR = 1.013; 95% CI = 0.993-1.034; P = .210). There was no heterogeneity and horizontal pleiotropy in the MR analyses (P > .05). PA is genetically and causally associated with higher risks of AA and AD. More attention should be paid to the screening and treatment of PA to reduce the incidence of aortic diseases.
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Registered trials
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