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Abstract Membranous nephropathy is the most common cause of the nephrotic syndrome in adults, accounting for about one third of cases . Membranous nephropathy can be secondary to other diseases, like immune diseases as systemic lupus erythematosus (SLE) , infections,like hepatitis B ,drugs like gold, penicillamine and non steroidal anti-inflammatory drugs (NSAIDS)or can occur in relation to a malignancy . In about two thirds of cases , however , no obvious etiologic agent or condition can be identified and the disease is called idiopathic . The natural history of patients with idiopathic membranous nephropathy varies from a spontaneous complete remission of proteinuria to rapid progression to end-stage renal disease. MGN (idiopathic disease) has a male and adult predominance with the peak incidence between 30 and 50 yr and MGN is particularly likely in patients over 50 yr of age who present with nephrotic syndrome . Membranous nephropathy is an immunologically mediated disease in which immune complexes deposit in the subepithelial space . The hallmark of MGN is subepithelial deposition of immunoglobulin G (IgG) together (in idiopathic MGN) with normal cellularity of the glomerular tuft . Antigen-antibody complexes can develop by the production of immune complexes in situ or by deposition . The antigens associated with primary membranous nephropathy are not known , it was recently demonstrated that antibodies (dipeptidyl-peptidase IV and neutral endopeptidase (NEP) which are expressed on the human podocytes, were produced by a pregnant woman and were transferred to her fetus , in which a severe form of membranous glomerulonephritis developed prenatally. |