ArticleFrontiers in nutrition2022
Genetic Evidence Supporting the Causal Role of Homocysteine in Chronic Kidney Disease: A Mendelian Randomization Study.
Article in Frontiers in nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- The causal role of homocysteine in multiple diseases: a systematic review of Mendelian randomization studies.Nutrition & metabolism · 2025Review
- Analysis of risk factors for abnormal renal function in patients with gout in Southwest China: a cross-sectional study.Rheumatology advances in practice · 2025Article
- Recent advances in the application of Mendelian randomization to chronic kidney disease.Renal failure · 2024Review
- The causal relationship between human brain morphometry and knee osteoarthritis: a two-sample Mendelian randomization study.Frontiers in genetics · 2024Article
- Genetically predicted adiponectin causally reduces the risk of chronic kidney disease, a bilateral and multivariable mendelian randomization study.Frontiers in genetics · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The causal relationship between homocysteine (Hcy) levels and chronic kidney disease (CKD) remains unclear. This study was performed to estimate the potential causal effects of Hcy on the estimated glomerular filtration rate (eGFR) and CKD. Materials and Methods: The single nucleotide polymorphisms (SNPs) associated with one standard deviation (SD) Hcy increase were identified using the genome-wide association study (GWAS). The summary statistics of the eGFR and CKD were from the CKDGen project in the European ancestry and the Population Architecture using Genomics and Epidemiology (PAGE) project in the non-European ancestry. Two-sample Mendelian randomization (MR) analyses were used in this study to verify the causal effects among Hcy, eGFR, and CKD. Results: The results showed that 1-SD Hcy increase was causally associated with eGFR decline in the CKDGen project (β = -0.027 log ml.min Conclusion: Using genetic data, Hcy increase is causally associated with renal function injury and further CKD.
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