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An Autoantibody Mechanism for Membranous Glomerulonephritis Due to Renal Vein Obstruction.

Arthur Copek; Robert C. Muehrcke, M.D., F.A.C.P.; Anil Mandal, M.D.; and Samuel Gotoff, M.D.
Ann Intern Med. 1968;68(5):1179-1180. doi:10.7326/0003-4819-68-5-1179_3
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Unilateral renal vein thrombosis produces massive proteinuria and in time the nephrotic syndrome. Bilateral membranous glomerulonephritis and subsequent progressive renal failure may develop as sequels. Serial clinicopathological studies were designed to investigate the pathogenesis of membranous glomerulonephritis due to renal vein occlusion.

The pathogenesis and evolution of renal lesions were studied in three patients by serial renal biopsies using light, electron, and immunomicroscopy. Tissue fixed for electron microscopy was cut at 0.5 µ, stained with methylene blue-azure II, and quantitatively analyzed. Individual glomerular cells were counted. Glomerular, Bowman's, and tubular basement membrane thicknesses were measured by electron microscopic analysis.



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