Role of 'catalytic' iron in an animal model of minimal change nephrotic syndrome.

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.