Key result
Genetically predicted higher serum uric acid increased hypertension risk (OR 1.215, 95% CI 1.119-1.320), while hypertension also increased serum uric acid (OR 1.018) with 27.3% mediation via BMI.
Why the study?
Does genetically predicted serum uric acid have a bidirectional causal relationship with hypertension in European populations, and does body mass index mediate this relationship?
Does genetically predicted serum uric acid have a bidirectional causal relationship with hypertension in European populations, and does body mass index mediate this relationship?
Answers are grounded in this paper and cite their sources.
Demonstrates a bidirectional genetic causal loop between serum uric acid and hypertension in Europeans with BMI partially mediating the effect of hypertension on uric acid, supporting integrated management of blood pressure, uric acid, and weight.
Background: Hypertension (HTN) may influence other chronic diseases, and a bidirectional relationship between HTN and serum uric acid (SUA) has been suggested, but evidence is insufficient. Body mass index (BMI) is associated with both HTN and SUA levels and may mediate their causal relationship. This study investigates the bidirectional causal relationship between HTN and SUA levels and the mediating effects of BMI. Methods: The two-sample bidirectional and mediation Mendelian randomization (MR) studies were conducted. In the first part, we conducted the univariable and multivariable bidirectional MR analyses. In the second part, BMI was included in the MR analyses as a mediator. Summary data on HTN, SUA, and BMI were obtained from the FinnGen, GWAS Catalog, and IEU OpenGWAS database. Results: The sample sizes of the European population included in analyses were 478,149 individuals for HTN, 343,836 for SUA, and 99,998 for BMI. In the European population, genetically predicted higher SUA was associated with increased HTN risk (OR = 1.215; 95% CI: 1.119 ∼ 1.320). HTN had an effect on SUA (OR = 1.018; 95% CI: 1.003 ∼ 1.033), in which the indirect effect via BMI showed an estimate of 0.006 (95% CI, 0.002 ∼ 0.010) with the mediated proportion of 27.3% (95% CI, 5.6% ∼ 48.9%). Conclusion: A bidirectional relationship between SUA and HTN was identified in the European population, with BMI partially mediating the effect of HTN on SUA.
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Shu et al. (2026) studied Hypertension and serum uric acid levels (n=478,149). Genetically predicted higher serum uric acid (SUA) and hypertension (HTN) vs. Lower genetically predicted SUA / normotensive controls was evaluated on Bidirectional causal risk of hypertension (HTN) and elevated serum uric acid (SUA) adjusted for BMI (OR 1.215, 95% CI 1.119-1.320, p=<0.05). Genetically predicted higher serum uric acid increased hypertension risk (OR 1.215, 95% CI 1.119-1.320), while hypertension also increased serum uric acid (OR 1.018) with 27.3% mediation via BMI.
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