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
CHURG J, MAUTNER W, GRISHMAN E, EISNER GM. Structure of Glomerular Capillaries in Proteinuria. Arch Intern Med. 1962;109(1):97–115. doi:10.1001/archinte.1962.03620130099011
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