ender and ethnic groups.
Pathogenetic mechanisms of IgA nephropathy are not completely understood; multiple mechanisms participate in both the primary and secondary forms. In general, pathogenesis is considered to be immune-complex mediated glomerulopathy, resulting in glomerular deposition of circulating IgA immune complexes. Studies revealed mesangial deposits of IgA. Mesangial deposits of IgA have been observed in 50 percent of patients with the disease; questions regarding polymeric versus monomeric IgA in the mesangium are relevant for the induction of the inflammatory response in the glomerular damage (polymeric is more active than monomeric).
Increases in the levels of IgA1 and IgA1-containing immune complexes in the circulation may be part of the pathogenesis of IgA nephropathy; this may be caused by decreased catabolism or increased synthesis. Studies with patients reach conflicting results, however agreement is found regarding increased production of IgA in patients. Cell cultures demonstrate increased production of IgA with a shift in the IgA subclass ratio toward IgA1, thus IgA1 appears to be central to the pathogenesis. IgA nephropathy patients are associated with mucosal infections and episodes of macroscopic hematuria, suggesting that the increased IgA may be localized in the mucosal tissues. Studies demonstrate increased functioning of helper T cells and decreased functioning of suppressor T cells. Cytokines may increase production of IgA.
Reasons for the mesangial deposition of IgA are still unknown, however, this action appears to be important regarding pathogenesis. Mesangial cells actively participate in the pathogenesis of IgA nephropathy, they appear to express surface receptors for IgA that facilitate accumulation of the IgA, and they synthesize an array of inflammatory cytokines and their cell su
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