Evidence map›Paper›PMID 41995538›Full record

ArticleMedicine2026

Extensive peripheral immune cell phenotypes and nephrotic syndrome: Tracing causality through genetics - a bilateral Mendelian randomization study.

Qiong Liu, Guojun Liang

Abstract read
In one paragraph

Article in Medicine, 2026. 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
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1 · What the graph read from it

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.

2 · The registry

The trial behind it

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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

2 authors.

Qiong LiuHuadu District People's Hospital of Guangzhou, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephrotic syndrome (NS) is a complex renal disorder characterized by significant proteinuria, hypoalbuminemia, and hyperlipidemia. While its etiology involves genetic and environmental factors, the role of the immune system in NS's pathogenesis remains incompletely understood. We adopted a bilateral Mendelian randomization approach, leveraging genetic variations as proxies to explore the causality between immune cell traits and NS. Utilizing genetic data sourced from the genome-wide association studies Catalog and FinnGen's database, we analyzed the association of 731 immune phenotypes with NS. Instrumental variables were selected based on stringent criteria, and the analysis was augmented by the inverse-variance weighting method, alongside sensitivity analyses to assess the robustness of our findings. Our analysis identified a significant causal association between CD8br natural killer T cell absolute cell count and NS, suggesting a novel immune-related risk factor for NS. In addition, decreased levels of 8 kinds of regulatory T cell phenotypes were observed in NS onset, suggesting a broader immunological impact of NS. These findings were supported by sensitivity analyses, which confirmed the stability and validity of the identified causal relationships. This pioneering study highlights the significant role of specific immune cell traits in the pathogenesis of NS, offering new insights into its immunopathological mechanisms. Future research should aim to elucidate the biological mechanisms underlying these associations and explore their implications across diverse populations to enhance the generalizability and applicability of these insights.

Indexed as

Mendelian Randomization AnalysisNephrotic SyndromeGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPhenotypePolymorphism, Single NucleotideT-Lymphocytes, Regulatorygenome-wide association studiesimmune cellMendelian randomizationnephrotic syndromesingle-nucleotide polymorphisms

Identifiers

PMID41995538
PMCPMC13095315

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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 OpenQuestion graph.