Idiopathic membranous nephropathy: Evolution in understanding the problem


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Abstract

The review highlights the evolution of ideas on the mechanisms responsible for the development of membranous nephropathy (MN), glomerulopathy that is the most common cause of nephrotic syndrome in adults. Primary emphasis is placed on the primary form of MN. The important step to understanding the nature of this clinical and morphological form of glomerulonephritis is to create its animal model (Heymann nephritis), then to decipher the mechanisms of immune complex damage (complement activation, a role of cellular immunity), and to identify autoantigens responsible for the development of idiopathic MN in man (podocyte neutral endopeptidase, transmembrane M-type phospholipase A2 receptor, thrombospondin type-1 domain-containing 7A. The findings constituted the basis for developing current methods for the diagnosis and treatment of MN, including the pathogenetically sound inhibition of autoantibody production, as well as a molecular orientation effect on podocyte dysfunction.

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