Abstract
Of 120 cases with primary, fatal glomerular lesions revereled in 7000 serial autopsy materials during the past 15 years, only 3 patients had died from membranous glomerulonephritis. The first patient had suffered for severe nephrotic syndrome for 3 years before his death, and rapidly developed fatal outcome due to acute renal failure. The autopsy revealed severe cellular cresentic glomerulonephritis superimposed on the membranous glomerulonephritis. GBM were electron microscopically diffusely thickend by large number of dense and/or translucent deposits in epimembraneum, without mesangial cells proliferation. The rapidly progressed renal failure had been followed these severe extracapillary (crescentic) glomerulonephritis. The second patient died from complicating pyelonephritis after 7 years from initial manifestation of membranous glomerulonephritis. Necropsy revealed considerable, inflammatory cell infiltration in interstitum, and about 51% obsolescent glomeruli concentrating on the outer cortex in which they may be induced by ischemic renal flow. Residual glomeruli electron microscopically revealed number of dense and/or translucent in the epimembraneum. Mesangial cells, however, did not increase in number. The third patient had had a history of nephrotic syndrome, DM and hypertension, since 111 years, and was admitted with fever, icterus and anasarca. She was suddenly developed fatal renal failure after drip inf usioncholangiography. Autopsy findings comprised diabetic and hypertensioe glomerular lesions overlapped membranous glomerulonephritis which was also electron microscopically comfirmed. Causes of the death of all three patients were not of membranous glomerulonephritis itself, but their complications may lead to fatal outcome, that is, superimposed severe crescentic glomerulonephritis, pyelonephritis or jaundice, DM and hypertension, as aggravating factors. Thus, the prognosis of membranous glomerulonephritis itself seems to be very favorable.
