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IgA Nephropathy: Recent Views on Pathogenesis and Treatment

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Nephrology

Summary

In many parts of the world, IgA nephropathy is one of the most common types of glomerulonephritis. The aim of this lecture is to summarize recent views on the pathogenesis of this disease and to evaluate current treatment in various countries.

The pathogenesis of IgA nephropathy has been investigated primarily in human patients because of the lack of appropriate animal models. It is generally agreed that IgA nephropathy is mediated by circulating IgA-dominant immune complexes which are deposited in the glomeruli. The formation of IgA-dominant immune complexes is likely to be enhanced by genetic factors which promote in vivo production of IgA. The enhancement of IgA production in this disease leads to the formation of various IgA-class autoantibodies. Nonimmunological factors, including various mediators, blood coagulation, and hemodynamic alterations, may cause exacerbation of this disease.

No specific treatment is known to improve the clinical course of IgA nephropathy. Current treatment is aimed at preserving renal functions and stabilizing associated symptoms such as hypertension. The selection of treatment protocols depends on the histopathological findings of renal biopsy specimens, which, so far, provide the most reliable parameters for predicting the prognosis in each patient. The drugs most widely used for treatment of IgA nephropathy are anti-platelet agents. Administration of corticosteroids is more effective for the preservation of renal function in patients with moderate levels of proteinuria than in those with severe proteinuria. Other types of treatment have not been evaluated by multi-center, double-blind studies. Despite relatively high rates of recurrence, transplantation is not contraindicated in the treatment of patients with IgA nephropathy.

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Sakai, H. (1991). IgA Nephropathy: Recent Views on Pathogenesis and Treatment. In: Hatano, M. (eds) Nephrology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-35158-1_4

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