Hagstrom G L, Bloom P M, Yum M N, Lavelle K J, Luft F C
Nephron. 1979;24(3):127-33. doi: 10.1159/000181700.
In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
为了研究铁蛋白诱导的肾小球肾炎发展过程中与蛋白质 - 铁复合物无关的蛋白质部分的作用,我们比较了铁蛋白、等摩尔量的脱铁铁蛋白和等摩尔量的右旋糖酐铁对瑞士白化小鼠的影响。将结果与注射生理盐水的对照组和未注射的对照组进行比较。铁蛋白导致了与免疫复合物主要沉积于系膜相关的肾小球肾炎。肾小管间质也出现了变化。右旋糖酐铁导致了类似但较轻的肾小管间质变化,且未引起肾小球改变。脱铁铁蛋白导致了通常与膜性沉积物相关的免疫复合物性肾小球肾炎。未出现肾小管或间质变化。接受脱铁铁蛋白的动物出现了蛋白尿。由于蛋白质 - 铁复合物会引起肾小管和间质损伤,脱铁铁蛋白可能提供了一个更合适的免疫复合物介导的肾小球肾炎模型。