title: Kidney iron status in passive Heymann nephritis and the effect of an iron-deficient diet.
abstract: 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.
authors.affiliation: Department of Pediatrics, Mississippi State University School of Medicine, Jackson, USA.
authors.forename: R
authors.initials: R
authors.lastname: Baliga
authors.forename: N
authors.initials: N
authors.lastname: Ueda
authors.forename: S V
authors.initials: SV
authors.lastname: Shah
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000633:toxicity; D000941:Antigens / Q000276:immunology; D004195:Disease Models, Animal; D015433:Glomerulonephritis, Membranous / Q000139:chemically induced / Q000150:complications / Q000378:metabolism*; D006486:Hemosiderosis / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D007116:Immunization, Passive; D007501:Iron / Q000008:administration & dosage / Q000378:metabolism*; D000090463:Iron Deficiencies; D019266:Iron, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D007668:Kidney / Q000378:metabolism*; D007672:Kidney Cortex / Q000737:chemistry; D007684:Kidney Tubules / Q000737:chemistry; D008099:Liver / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D019266:Iron, Dietary; C035812:renal tubular antigen; D008315:Malondialdehyde; D007501:Iron