Authors
Xin Liu, Wenwen Yang
Published in
Medicine. Volume 105. Issue 44. Pages e51095. Oct 30, 2026.
Abstract
Renal failure significantly impairs the kidneys' ability to filter waste and maintain fluid balance. This study employed Mendelian Randomization (MR) to investigate the causal effect of BMI on 44 biomarkers related to renal failure. The genetic data were sourced from publicly available genome-wide association studies (GWAS) and biobank datasets, including blood cells, urinary electrolytes, enzymes, liver markers, lipids, and blood pressure. Single-nucleotide polymorphisms (SNPs) were used as instrumental variables (IVs) to assess the causal relationships and to identify significant mediators of the BMI-renal failure pathway. The study found that BMI is a risk factor for renal failure (OR = 1.324, P = .00185). Out of 44 biomarkers, nine were associated with renal failure, and five acted as mediators in the relationship between BMI and renal failure: cystatin C (12.34%), glucose (7.02%), glycated hemoglobin (HbA1c) (6.83%), diastolic blood pressure (6.37%), and systolic blood pressure (7.14%). The findings suggest that reducing BMI could improve renal health by addressing metabolic factors like blood glucose and blood pressure. This study highlights the causal pathways linking BMI to renal failure, underscoring the importance of weight management and metabolic control for prevention.
PMID:
43012814
Bibliographic data and abstract were imported from PubMed on 11 Nov 2026.
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