Gluten and IgA nephropathy: you are what you eat? (1)
IgA derived from mesangial deposits is typically of the IgA1 isoform, polymeric, and poorly galactosylated in its hinge region compared with that found in healthy individuals’ serum. There has also been long-standing interest in the potential links between bowel disease and IgA nephropathy. Celiac disease and inflammatory bowel disease have been implicated as secondary causes of IgA nephropathy.
In mice, IgA deposition could be induced by the addition of exogenous antigens to the diet. Mice placed on the gluten- containing or gliadin-enriched diet displayed significantly greater IgA deposition compared with those on the gluten-free diet, with increased anti- gliadin IgA found in the serum and glomerular deposit eluates.
4% of patients with IgA nephropathy were found to have either previously or newly diagnosed celiac disease, compared with an estimated prevalence of 0.5–1% in the general population.
Anti-gliadin antibodies in patients with IgA nephropathy demonstrate remarkable variation, ranging from 3% to as high as 70% of cohorts studied, with differences previously attributed to assay methodology, small sample sizes, and different population groups.
An enhanced or exaggerated inflammatory response to gluten may drive this, leading to antigen access to the systemic circulation, driving production of the pathogenic poorly galactosylated form of IgA that then deposits in the mesangium.
