Evidence map›Paper›PMID 41728059›Full record

ArticleKidney diseases (Basel, Switzerland)

The Impact of Gut Microbiota on Immunoglobulin A Nephropathy through the Mediation of Specific Immune Cells: A Mendelian Randomization Study.

Junli Wan, Mei Yang, Qilin Chen, Shuying Li, Xinyi Ye, Qiu Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Kidney diseases (Basel, Switzerland). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Junli WanDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.
Mei YangDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.
Qilin ChenDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.
Shuying LiDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.
Xinyi YeDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.
Qiu LiDepartment of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Disease, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Gut microbiota alterations had been implicated in the pathogenesis of IgA nephropathy (IgAN). However, how did the gut microbiota participated in the onset and development of IgAN was unclear. This study investigated the causal effects of gut microbiota on IgAN and identifies potential mediators, including lipids, inflammatory factors, metabolites, and immune cells. Methods: Genome-wide association study (GWAS) data for gut microbiota, IgAN, and mediators were analyzed. Two-sample Mendelian randomization (MR) assessed the causal relationship between gut microbiota and IgAN, followed by two-step MR mediation analysis to identify indirect effects via mediators. Mediation effects were quantified using the coefficient product method. Results: MR analysis identified six genera and one phylum of gut microbiota with potential causal linked to IgAN. Two-step MR revealed one lipid, two inflammatory factors, ten metabolites, and sixteen immune cell types as mediators. Specifically, Conclusion: Gut microbiota alterations could causally influence IgAN, with specific immune cell subsets mediating these effects. Specific subsets of B cells and T cells could be involved in the development of IgAN, which would need our attention in the future.

Indexed as

Gut microbiotaIgA nephropathyImmune cellsMendelian randomization

Identifiers

PMID41728059
PMCPMC12923258

What Socratic holds

Textmetadata
LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.