Korean Journal of Nephrology 1989;8(1):7-18.
퓨로마이신 아미노누클레오사이드 신증에서 사구체 기저막 음이온부위의 초기변화
박문수 , 최용 , 고광욱
Abstract
Puromycin aminonucleoside (PAN) nephrosis has been studied as an animal model of human minimal change nephrotic syndrome, however its mechanism of proteinuria is not elucidated clearly. Recently it was found that there are certain fixed, negatively-charged structures, I.e. anionic sites, in the glomerular basement membrane and it was proved by physiological experiment that they restrict the filtration of negatively-charged macromolecules like albumin. The changes of GBM anionic sites in PAN nephrosis have been reported by many authors but the results have varied according to the cationic marker used. The foot process fusion, a well-known electron micro- scopic feature in minimal change nephrotic syndrome, is thought to be related to the loss of sialoprotein in the glomerular epithelial cell surface, but its relation to proteinuria remains unresolved. To find out whether the changes in GBM anionic sites and foot processes are preceding events or secondary phenomenon to proteinuria, the author induced PAN nephrosis in 30 Wistar rats and recorded quantitatively the sequential changes in the GBM anionic sites and the widths of the foot processes. Then these findings were compared with those in 5 control rats. GBM anionic sites were stained with polyethyleneimine (PEI), a cationic marker, in this study. Twenty four hours after administration of PAN, there was a statistically significant decrease in the number of GBM anionic sites compared with the control group (15. 4?1.6 versus 19.5?2.0 per GBM 1,000nm,p<0.05). This change in the number of GBM anionic sites preceded, was directly reflected in, the increase in urinary albumin excretion, which began 36-48 hours after PAN injection. The widening of foot process was observed 72 hours after PAN injection. These findings suggest that GBM anionic sites play an important role as a charge barrier, and that the proteinuria appear as a result of an alteration in this charge barrier. Considering the timing of the foot process fusion, the author believes that it is a secondary phenomenon or an epiphenomenon rather than the cause of proteinuria.
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