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JACOB CHURG, M.D.; WILLY MAUTNER, M.D.; EDITH GRISHMAN, M.D.; GILBERT M. EISNER, M.D.

Arch Intern Med. 1962;109(1):97-115.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The appearance of large quantities of protein in the urine has long been associated with changes in the renal architecture, although the precise lesion or lesions responsible for this abnormality are not clearly understood. Normally some protein is filtered at the glomerulus and reabsorbed by the tubules. Several investigators have therefore suggested that urinary protein loss is due to failure of the tubular reabsorptive mechanism.¹ The majority, however, has attributed the development of proteinuria to increased permeability of glomerular capillaries to plasma proteins.² Before the advent of electron microscopy, those who held this view could correlate proteinuria only with a general disturbance of the glomerulus, as seen in acute or chronic glomerulonephritis or in diabetic glomerulosclerosis. Changes in the capillary walls, often observed with a light microscope, proved difficult to study and to evaluate.^3,4 The application of electron microscopy to biopsy specimens permitted much better visualization of . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

Present address: Department of Medicine, Georgetown University Hospital, Washington 7, D.C. (Dr. Eisner).; Department of Pathology, Cell Research Laboratory and Department of Medicine, The Mount Sinai Hospital, New York.

Footnotes
Submitted for publication Aug. 4, 1961.

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