Mesangial IgA nephritis.

Current data suggest that mesangial IgA nephritis is mediated by the mesangial deposition of soluble antigen-IgA class antibody complexes from the circulation. It is likely that common infectious gut flora and dietary antigens contribute to the immune complex load. Defects in antigen exclusion at the mucosa, in the control of IgA production, and in immune complex clearance are postulated to account for each of the recognized clinical syndromes. As yet no effective treatment is available, and a detailed analysis of the mediation pathways will be required before prevention or therapy can be attempted.