Summary
This Mendelian randomization study used genetic variants associated with circulating and toenail selenium levels from large GWAS datasets to assess causality between selenium status and kidney function in European populations. The analysis found that genetically predicted higher selenium levels were associated with decreased eGFR and increased BUN, suggesting a causal adverse effect of elevated selenium on kidney function. Sensitivity analyses detected no pleiotropy, supporting the robustness of the causal inference.
Regional applicability
The study used European-ancestry GWAS data and may have limited direct applicability to United Kingdom populations with different genetic ancestry or dietary selenium exposures, though genetic causal estimates are often transferable across European populations. The findings suggest selenium supplementation warrants cautious consideration in individuals with or at risk of kidney disease, irrespective of geography, but UK-specific dietary and clinical guidance would benefit from population-level confirmation.
Key measures
Estimated glomerular filtration rate (eGFR), blood urea nitrogen (BUN), genetically predicted circulating selenium levels, genetically predicted toenail selenium levels
Outcomes reported
The study assessed the causal relationship between genetically predicted selenium levels and kidney function markers (estimated glomerular filtration rate and blood urea nitrogen) using Mendelian randomization analysis in European-ancestry populations.
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