VICTOR E. POLLAK, M.D., F.R.C.P.(EDIN.); SEYMOUR ROSEN, M.D.; CONRAD L. PIRANI, M.D.; ROBERT C. MUEHRCKE, M.D., F.A.C.P.; ROBERT M. KARK, M.D., F.A.C.P., F.R.C.P.
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Twenty-one patient each with lipoid nephrosis (LN) and membranous glomerulonephritis (MGN) were observed for a long period of time. Six patients with LN and one with MGN were under 14 years of age. All 21 with LN and 17 with MGN had nephrotic syndrome; 4 with MGN had asymptomatic persistent proteinuria. LN and MGN could not be distinguished clinically or by laboratory tests. In LN, fusion of foot processes of glomerular visceral epithelial cells was the only significant finding in initial biopsies. Slight homogeneous thickening of the glomerular basement membrane developed later in 3 patients; no significant changes subsequently occurred in 9 patients. Three patients with LN died presumably of infection when edematous. An average of 5 years later the others were alive without renal functional impairment. The proteinuria decreased rapidly with prednisone treatment in 30 to 40 exacerbations. Continued prednisone treatment was needed in some but not all patients to prerecurrence of proteinuria.
In MGN mild to moderately severe thickening of the glomerular capillary basement membrane and extramembranous subepithelial deposits were found in initial biopsies. Serial studies demonstrated little change in the character or severity of the lesions. After an average of 5 years two patients had died. Thirteen had normal renal function, and in all the proteinuria was <2 g/day. Six patients were azotemic; all had persistent heavy proteinuria. There was no effect of prednisone on proteinuria, longevity, or renal function.
POLLAK VE, ROSEN S, PIRANI CL, et al. Natural History of Lipoid Nephrosis and of Membranous Glomerulonephritis. Ann Intern Med. 1968;69:1171–1196. doi: https://doi.org/10.7326/0003-4819-69-6-1171
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Published: Ann Intern Med. 1968;69(6):1171-1196.
Autoimmune Kidney Disease, Nephrology, Rheumatology.
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