ArticleRenal failure2025
Causal associations between circulating metabolites and chronic kidney disease: a Mendelian randomization study.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
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Who cites it
1 citing paper in PubMed.
- Emerging Urinary Biomarkers and Innovative Technologies for the Early Detection and Personalized Management of Chronic Kidney Disease.International journal of molecular sciences · 2026Review
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Authors and funding
3 authors.
Funding
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Abstract
backgroundCirculating metabolites have been associated with cross-sectional renal function in population-based research. Nevertheless, there is currently little proof to support the idea that metabolites either cause or prevent renal function. New treatment targets and ways to screen individuals with impaired renal function will be made possible
methodsWe assessed the causal relationship between 452 serum metabolites and six renal phenotypes (CKD, rapid progression to CKD [CKDi25], rapid eGFR decline [CKD rapid3], dialysis, estimated glomerular filtration rate, and blood urea nitrogen) using univariate Mendelian randomization, primarily employing the inverse variance weighted method with robust sensitivity analyses. Heterogeneity and pleiotropy were examined
resultsWe identified glycine and N-acetylornithine as potential causal mediators of CKD and renal dysfunction. Notably, lowering glycine levels may increase the risk of cholelithiasis and cholecystitis, while reducing N-acetylornithine could have unintended effects on tinnitus.
conclusionGlycine and N-acetylornithine represent promising therapeutic targets for CKD and renal function preservation, but their modulation requires careful risk-benefit assessment to avoid adverse effects.
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