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Membranous nephropathy. Insights from Heymann nephritis.

Membranous nephropathy, the most common cause of idiopathic nephrotic syndrome in the adult, results from immunological injury characterized by discontinuous granular deposits of immunoglobulins and complement components in the glomerular capillary wall.1 Human membranous nephropathy can be the pathological expression of various unrelated conditions, for example, infectious, neoplastic, toxic, and autoimmune,1 2 which suggests that diverse immune complex systems may cause tissue injury by a similar pathogenic mechanism. The condition is characteristically slow in progression; spontaneous remissions do occur, apparently during early stages of the disease, but nearly half of the patients develop renal insufficiency or end-stage renal disease over a period of 5 to 15 years,3 despite various modalities of therapy.34 In only a few instances of human membranous nephropathy has a putative antigen been identified; however, the mechanisms of tissue injury and factors that affect the progression of the disease are poorly understood. In contrast, studies in Heymann nephritis, an experimental model that resembles human membranous nephropathy, have yielded a wealth of information, mostly in the last 15 years; this information probably applies to the pathogenesis of human membranous nephropathy. What follows, a brief account of these developments, is intended to be focused, not exhaustive. For a comprehensive treatment of this subject the reader is referred to Kerjaschki's article.5 Heymann Nephritis Model: Antigenic Fractions