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Journal of the American Society of Nephrology, Vol 7, 1183-1188, Copyright © 1996 by American Society of Nephrology
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R Baliga, N Ueda and SV Shah
Department of Pediatrics, Mississippi State University School of Medicine, Jackson, USA.
In the study presented here, the iron status in the kidney in passive Heymann nephritis, a complement-dependent model of membranous nephropathy, was examined. To examine whether the effect of immune injury on iron status has a pathogenic role, the effect of an iron- deficient diet was also determined. Injection of the anti-Fx1A antibody (10 mg/100 g body wt) in Sprague-Dawley rats resulted in no change in the serum iron level, a marked increase in the urinary excretion rate of iron, a marked increase in non-heme iron content of kidney cortex, and a marked increase in the non-heme iron level in tubules. These increases in iron were prevented by feeding the rats an iron-deficient diet. In the rats fed a normal iron diet and injected with anti-Fx1A- lgG, there was no significant change in the non-heme iron level in glomeruli. However, an iron-deficient diet resulted in a significant decrease in the non-heme iron level in glomeruli, compared with its respective control. In addition, an iron-deficient diet significantly reduced urinary protein excretion rate (Day 5: iron-replete, 68 +/- 12 mg/24 h, N = 12; iron-deficient, 36 +/- 11, N = 10, P < 0.05) in the complement-dependent immune phase of the glomerular injury. Taken together, these data indicate a marked alteration in the iron status in the kidney and suggest an important role of iron in glomerular injury of passive Heymann nephritis.
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