Morphological alterations of glomerulus induced by infusion of cationized ferritin.

H Kubosawa, H Nakayama, T Sano, Y Kondo
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引用次数: 4

Abstract

Morphological alterations of the glomerulus were induced by infusion of cationized ferritin. After a direct injection of highly cationized ferritin (CF) into the left kidney of rats, endothelial injuries were followed by activation of platelets and the coagulation system after 1-2 h, which occluded capillary loops. In most glomeruli, resolving processes occurred from 2 h onward, leaving a mild thickening of the mesangial region at 7 days. On the other hand, in severely involved glomeruli, capillary loops were still obstructed even at 24 h by hypertrophic and proliferated endothelial cells as well as mesangial cells, instead of platelets and fibrin strands. After this period, exfoliation of podocytes and endothelial cells occurred over a wide area, which resulted in glomerular obsolescence at 7 days. These progressive glomerular injuries were assumed to be closely related to the persistence of CF in glomeruli, which might be caused by disturbances of glomerular clearing systems. Mild proteinuria was only noticed in severely involved cases. It is concluded that an assault on glomerular endothelial cells by cationic macro-molecules can cause thrombotic complications leading to glomerular obsolescence.

输注阳离子化铁蛋白所致肾小球形态学改变。
输注阳离子化铁蛋白可引起肾小球形态学改变。在大鼠左肾内直接注射高阳离子化铁蛋白(CF)后,内皮细胞损伤,1 ~ 2小时后血小板和凝血系统激活,毛细血管袢闭塞。在大多数肾小球中,溶解过程在2小时后发生,在7天时留下轻度的肾小球系膜增厚。另一方面,在严重受累的肾小球中,毛细血管袢即使在24小时仍被肥大和增殖的内皮细胞以及系膜细胞阻塞,而不是血小板和纤维蛋白链。在此之后,足细胞和内皮细胞大面积脱落,导致肾小球在第7天退化。这些进行性肾小球损伤被认为与CF在肾小球中的持续存在密切相关,这可能是由肾小球清除系统的紊乱引起的。轻度蛋白尿只在严重受累的病例中出现。由此可见,阳离子大分子对肾小球内皮细胞的攻击可引起血栓性并发症,导致肾小球退化。
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