Gut microbiota in IgA nephropathy; a letter to the editor on recent data

Gut dysbiosis and intestinal barrier dysfunction are thought to contribute to the progression of IgA nephropathy (IgAN) by enhancing the production of galactose-deficient IgA1, which leads to the formation of nephrotoxic immune complexes. Furthermore, metabolites generated by an altered gut microbiome—such as indoxyl sulfate and trimethylamine N-oxide—can impair the intestinal barrier and activate mucosal immunity, playing a causal role in the disease’s pathogenesis.

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Publication Details

Journal
Journal of Renal Endocrinology
Published
2025-06-08
DOI
https://doi.org/10.34172/jre.2025.25198
Citations
1
Primary Topic
Renal Diseases and Glomerulopathies
Type
article
Field-Weighted Citation Impact
1.43
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article

Gut microbiota in IgA nephropathy; a letter to the editor on recent data

Kamran Shirbache
1 citations
Journal of Renal Endocrinology
Renal Diseases and Glomerulopathies
1.43
article

Gut microbiota in IgA nephropathy; a letter to the editor on recent data

Kamran Shirbache
article en
1 citations

Abstract

Gut dysbiosis and intestinal barrier dysfunction are thought to contribute to the progression of IgA nephropathy (IgAN) by enhancing the production of galactose-deficient IgA1, which leads to the formation of nephrotoxic immune complexes. Furthermore, metabolites generated by an altered gut microbiome—such as indoxyl sulfate and trimethylamine N-oxide—can impair the intestinal barrier and activate mucosal immunity, playing a causal role in the disease’s pathogenesis.

Journal of Renal EndocrinologyVol. 11
Université Paris Cité (FR), Assistance Publique – Hôpitaux de Paris (FR), Hôpital Robert-Debré (FR)
Openalex Percentile: Top 19%
Renal Diseases and Glomerulopathies
1.43
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