Abstract
Resent advances in podocyte biology indicated that the main cause of the heavy proteinuria in nephrotic syndrome (NS) is a dysfunction of slit diaphragm. On the other hand, we need to consider the theory of charge selective barrier dysfunction of glomerular capillary wall (GCW) in NS, at the same time, because the charge selective barrier is not likely to have a place in slit diaphragm. Therefore we re-evaluated the charge selective barrier function in NS and chronic glomerulonephritis using recently established charge selectivity index (CSI) in comparison with Dent disease. CSI is a clearance ratio of IgG and IgA. In order to evaluate the CSI of normal glomerular filtrate, we measured the CSI of Dent disease. The urine of Dent disease is considered to be a concentrate of filtered protein from normal glomerulus, without having a process of tubular protein reabsorption. 35 patients with podocyte diseases, 72 patients with chronic glomerulonephritis and8patients with Dent disease, were analyzed. CSI (mean±SD) of Podocyte disesses, chronic glomerulonephritis and Dent disease was 1.12±0.25, 0.42±0.31 and 0.16±0.06 respectively. The results indicated that the charge selective barrier of GCW is working strongly in normal glomerulus, less strongly in podocyte diseases and not working in chronic glomerulonephritis. Taking into account for the known dysfunction of slit diaphragm in nephrotic syndrome, the true cause of nephrotic syndrome may affect to both slit diaphragm and GCW resulting in heavy proteinuria showing some degree of charge selectivity.
