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

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.