ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2024
IgA nephropathy: gut microbiome regulates the production of hypoglycosilated IgA1 via the TLR4 signaling pathway.
Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Risk Factors and Outcomes of Immunoglobulin A Vasculitis in Patients with Inflammatory Bowel Disease and vice versa: A Systematic Review of the current literature.Current gastroenterology reports · 2026Pooled it
- Visceral Obesity and Metabolic Dysfunction in IgA Nephropathy: Nutritional and Metabolic Perspectives on Disease Progression.Nutrients · 2025Pooled it
- Potential Roles of Escherichia coli in IgA Nephropathy: Evidence, Mechanistic Hypotheses and Microbiota-Targeted Strategies.Microbial biotechnology · 2026Review
- IgA nephropathy: an overview of the disease, its pathophysiology, and involvement of the gut-kidney axis.Kidney international supplements · 2026Review
- KMT5a-Mediated IRF3 Stabilization Enhances Macrophage Chemotaxis and Renal Fibrosis Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ELMO1 and Rac1 Signaling in Kidney Disease: Molecular Mechanisms, Context-Dependent Roles, and Therapeutic Potential.Biomedicines · 2026Review
- Gut Virome Characteristics and Network Alterations in IgA Nephropathy.Kidney international reports · 2026Article
- Review
- Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease.Frontiers in immunology · 2026Review
- Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy.Journal of immunology research · 2026Review
- Gd-IgA1-targeting therapy in IgA nephropathy ~what is pathogenic Gd-IgA1?~.Frontiers in nephrology · 2026Review
- Combined treatment withFrontiers in pharmacology · 2026Article
- Serum anti-β2 spectrin IgA antibodies are produced in a CD4 T cell-independent manner in IgA nephropathy model mouse.Frontiers in immunology · 2026Article
- Targeted release of budesonide modulates key gut microbial abnormalities in immunoglobulin A nephropathy.Frontiers in immunology · 2026Article
- Gut-kidney axis in IgA nephropathy: mechanisms linking microbiota dysbiosis to immune dysregulation, Gd-IgA1 generation, and renal injury.Frontiers in immunology · 2026Review
- The role of the gut-lung axis in persistent inflammation and disease progression in chronic obstructive pulmonary disease: mechanistic evidence and therapeutic implications.Frontiers in immunology · 2026Review
- Inflammatory bowel disease and renal disorders: from clinical associations to shared mechanisms and management strategies.Frontiers in immunology · 2026Review
- DietaryVeterinary world · 2026Article
- Microbiota-Gut-Kidney Axis and Targeted Therapeutic Strategies in Kidney Diseases.International journal of biological sciences · 2026Review
- The role of mucosal immune dysregulation in the pathogenesis of immunoglobulin A nephropathy.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 1 country.
Funding
Abstract
backgroundImmunoglobulin A nephropathy (IgAN) is a major cause of primary glomerulonephritis characterized by mesangial deposits of galactose-deficient IgA1 (Gd-IgA1). Toll-like receptors (TLRs), particularly TLR4, are involved in the pathogenesis of IgAN. The role of gut microbiota on IgAN patients was recently investigated. However, whether gut microbial modifications of Gd-IgA1 through TLR4 play a role in IgAN remains unclear.
methodsWe recruited subjects into four groups, including 48 patients with untreated IgAN, 22 treated IgAN patients (IgANIT), 22 primary membranous nephropathy and 31 healthy controls (HCs). Fecal samples were collected to analyze changes in gut microbiome. Gd-IgA1 levels, expression of TLR4, B-cell stimulators and intestinal barrier function were evaluated in all subjects. C57BL/6 mice were treated with a broad-spectrum antibiotic cocktail to deplete the gut microbiota and then gavaged with fecal microbiota transplanted from clinical subjects of every group. Gd-IgA1 and TLR4 pathway were detected in peripheral blood mononuclear cells (PBMCs) from IgAN and HCs co-incubated with lipopolysaccharide (LPS) and TLR4 inhibitor.
resultsCompared with the other three groups, different compositions and decreased diversity demonstrated gut dysbiosis in the untreated IgAN group, especially the enrichment of Escherichia-Shigella. Elevated Gd-IgA1 levels were found in untreated IgAN patients and correlated with gut dysbiosis, TLR4, B-cell stimulators, indexes of intestinal barrier damage and proinflammatory cytokines. In vivo, mice colonized with gut microbiota from IgAN and IgANIT patients mimicked the IgAN phenotype with the activation of TLR4/MyD88/nuclear factor-κB pathway and B-cell stimulators in the intestine, and had with enhanced proinflammatory cytokines. In vitro, LPS activated TLR4/MyD88/NF-κB pathway, B-cell stimulators and proinflammatory cytokines in PBMCs of IgAN patients. This process may induce the overproduction of Gd-IgA1, which was inhibited by TLR4 inhibitors.
conclusionsOur results illustrated that the gut-kidney axis is involved in the pathogenesis of IgAN. Gut dysbiosis could stimulate the overproduction of Gd-IgA1 via TLR4 signaling pathway production and B-cell stimulators.
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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.