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Just over 50 years ago, the late David Jones1 identified (using the periodic acid–Schiff and methenamine silver stains) the unique glomerular pathologic features of membranous nephropathy, thus distinguishing it from other causes of “nephrotic glomerulonephritis.” Subsequent immunofluorescence and electron-microscopical studies established that membranous nephropathy was also characterized by striking granular aggregations of IgG and electron-dense deposits along the outer (or subepithelial) aspect of the glomerular basement membrane. These glomerular IgG deposits were initially believed to represent an accumulation of immune complexes arising from the circulation, as is found with glomerulonephritis in a rabbit model (chronic serum sickness).In 1959, Heymann . . .
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Richard J. Glassock (2009) studied this question.
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