The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis. A light and electron microscopic study using horseradish peroxidase and ferritin as tracers.
The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis in rabbits was studied by light and electron microscopy using horseradish peroxidase (effective radius 30 A; mol. wt. 40,000) and ferritin (effective radius 60 A; mol. wt. 480,000) as protein tracers. It was found that more ferritin, but paradoxically, less horseradish peroxidase gained access to the urinary space. Observations made by electron microscopy appeared to indicate a decreased permeability of most part of the damaged glomerular capillary wall to both tracers. These results favor the interpretation that proteinuria in chronic serum sickness glomerulonephritis is the result of focal rather than diffuse increase in permeability of the glomerular capillary wall. Lesions of segments of the nephron other than the glomerular capillary wall, may contribute to the leakage of proteins to the urinary space.
D000818:Animals; D002199:Capillary Permeability; D002908:Chronic Disease; D005260:Female; D005293:Ferritins; D005921:Glomerulonephritis / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006735:Horseradish Peroxidase; D007678:Kidney Glomerulus / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D011507:Proteinuria / Q000473:pathology* / Q000503:physiopathology; D011817:Rabbits; D012713:Serum Sickness / Q000150:complications
D005293:Ferritins; D006735:Horseradish Peroxidase