Membranous nephropathy is the most common cause of nephrotic syndrome in adults in developed countries. This renal disease affects males more than females.
The term membranous refers to the thickening of the capillary walls of the glomeruli as seen on light microscopy. The thicken-ing appears to be seen on the epithelial side of the basement membrane where electron-dense deposits can be found. These deposits appear to represent in situ formation or deposition of immune com-plexes. Immunofluorescence studies show granular deposits of IgG and C3 (including the membrane attack complex) along the capillary walls. There is minimal mesan-gial involvement. In about 75–80 percent of cases, the disease is idiopathic. Second-ary causes are associated with systemic lupus erythematosus (SLE), malignancy, infections (hepatitis B and C viruses and syphilis), and drugs (gold, penicillamine, mercury compounds, tiopronin, capto-pril, diclofenac, and other nonsteroidal agents).
The presence of subepithelial deposits suggests that the offending antigen may be cationic in its charge to be able to cross the anionic GBM. Antibodies to endogenous antigens (e.g., megalin or gp 330) have been implicated in the Heymann nephri-tis model of membranous nephropathy. Megalin appears to function as a receptor for aminoglycosides, advanced glycation products, and vitamin D.
The benign course of idiopathic membranous nephropathy has led clinicians to withhold treatment. About 5 to 20 percent of cases go into spontaneous remission with-out treatment. Partial remissions (<2 g/day proteinuria) can be seen in another 25 to 40 percent of cases. However, if progressive renal disease is noted, use of steroids and cytotoxic agents are recommended. Treat-ment of secondary membranous nephrop-athy involves treatment of the underlying disease (e.g., treatment of malignancy) or withholding offending drugs.