Electron microscopic studies on human renal biopsies. The structural basis of proteinuria
The structural alterations as observed with conventional histopathological techniques in human glomeruli obtained from patients with diseases characterized by marked proteinuria are varied. Glomeruli from such individuals may appear either within normal limits as in lipid nephrosis or else are characterized by marked thickening of the glomerular capillary walls as in chronic glomerulonephritis or amyloidosis of the kidney. These findings are rather contradictory and provide no structural basis for understanding the marked increase in permeability to plasma proteins of the glomeruli in such diseases. In order to further elucidate this problem, a study was undertaken of the fine structure of the human glomerulus obtained from biopsy material in various conditions associated with proteinuria. Nine cases of proteinuria were studied: two of juvenile lipid nephrosis, three of membranous glomerulonephritis, two of subacute and chronic glomerulonephritis, and two of amyloidosis. Marked proteinuria with a nephrotic syndrome was exhibited by one of the patients with lipid nephrosis, by one of the patients with membranous glomerulonephritis, and by both of the amyloid cases. The observations indicate that the structural basis of proteinuria is the presence of defects in the basement membrane of the glomerular capillary wall. This observation was previously reported in more detail in a study which consisted of some of the material included here (1).
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