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Title: Role of 'catalytic' iron in an animal model of minimal change nephrotic syndrome. Author: Ueda N, Baliga R, Shah SV. Journal: Kidney Int; 1996 Feb; 49(2):370-3. PubMed ID: 8821819. Abstract: Treatment of minimal change disease, like most glomerulonephritides, is empirical because underlying mechanisms that cause glomerular injury are not known. We examined a pathogenic role of 'catalytic' iron in a model of minimal change nephrotic syndrome induced by injection of puromycin aminonucleoside (7.5 mg/100 g body wt) to rats. Although there was no significant change in non-heme iron content in glomeruli, the bleomycin-detectable iron (capable of catalyzing free radical reactions) was markedly increased in glomeruli from nephrotic rats when compared to control. In contrast, despite a marked and significant increase in the non-heme iron content in tubules, there was no significant change in the bleomycin-detectable iron in tubules from nephrotic rats. In a separate in vivo study, the iron chelator, deferoxamine, prevented the increase in the bleomycin-detectable iron in glomeruli and provided complete protection against proteinuria. Taken together, our data suggest an important pathogenetic role for glomerular catalytic iron in the puromycin aminonucleoside-induced minimal change nephrotic syndrome.[Abstract] [Full Text] [Related] [New Search]