Studies on the Glomerular Permeability with Human Liver Ferritin

To clarify the roles of the glomerular basement membrane (GBM) in filtration mechanisms, human liver ferritin was used for the first time as a tracer. Urinary excretion of human liver ferritin was measured and the injected ferritin was tracked under electron microscopy. Puromycin aminonucleoside (PAN) nephrosis was induced in Sprague Dawley rats and normal saline was injected into control rats. Monomeric and polymeric human ferritin were isolated from post mortem samples. Both kinds of human liver ferritin were injected into the experimental and control rats and urine samples were examined for human ferritin by radioimmunoassay. Rats with PAN nephrosis excreted approximately 33 times more monomeric ferritin than the controls. Appreciably more monomeric ferritin was excreted than polymeric ferritin. In control rats, monomeric ferritin particles were restricted in the lamina rara interna and inner aspect of the glomerular basement membrane 30 min after injection. On the other hand, in rats with PAN nephrosis, monomeric ferritin particles were seen throughout the width of the GBM and in the epithelial cells. With human liver ferritin, we were able to demonstrate the escape of the ferritin into the urine in addition to conducting the conventional electron microscopic tracer study of the glomerular capillary wall. Human liver ferritin shows potential as a useful tracer in the study of glomerular permselectivity.