ArticleFrontiers in genetics2021
Causal Inference Between Chronic Periodontitis and Chronic Kidney Disease: A Bidirectional Mendelian Randomization Analysis in a European Population.
Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Genetic evidence for causal link between systemic inflammation and dental caries risk: A bidirectional Mendelian randomization study.Medicine · 2026Article
- A Causal Association Study Between Chronic Kidney Disease and Oral Health: A Mendelian Randomization Study.Health science reports · 2025Article
- Exploring and validating associations between six systemic inflammatory indices and ischemic stroke in a middle-aged and old Chinese population.Aging clinical and experimental research · 2025Article
- The Genetic Cross-Talk between Periodontitis and Chronic Kidney Failure Revealed by Transcriptomic Analysis.Genes · 2023Article
- Chronic Kidney Disease and Periodontitis Interplay-A Narrative Review.International journal of environmental research and public health · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious epidemiological studies have shown significant associations between chronic periodontitis (CP) and chronic kidney disease (CKD), but the causal relationship remains uncertain. Aiming to examine the causal relationship between these two diseases, we conducted a bidirectional two-sample Mendelian randomization (MR) analysis with multiple MR methods.
methodsFor the casual effect of CP on CKD, we selected seven single-nucleotide polymorphisms (SNPs) specific to CP as genetic instrumental variables from the genome-wide association studies (GWAS) in the GLIDE Consortium. The summary statistics of complementary kidney function measures, i.e., estimated glomerular filtration rate (eGFR) and blood urea nitrogen (BUN), were derived from the GWAS in the CKDGen Consortium. For the reversed causal inference, six SNPs associated with eGFR and nine with BUN from the CKDGen Consortium were included and the summary statistics were extracted from the CLIDE Consortium.
resultsNo significant causal association between genetically determined CP and eGFR or BUN was found (all
conclusionEvidence from our bidirectional causal inference does not support a causal relation between CP and CKD risk and therefore suggests that associations reported by previous observational studies may represent confounding.
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