Kinoue K, Hattori M, Horita S, Kawaguchi H, Ito K
Department of Pediatric Nephrology, Tokyo Wemen's Medical College, Japan.
Nihon Jinzo Gakkai Shi. 1996 Aug;38(8):364-71.
There is a strong association between epithelial crescent formation and the outcome of patients with Henoch-Schönlein purpura nephritis (HSPN), but little is known about the mechanisms of crescent formation in this disease. In this study, we examined whether or not glomerular endocapillary proliferation, fibrinoid necrosis and infiltrating inflammatory cells are involved in the process of crescent formation. Renal biopsy specimens were obtained from 19 patients (11 males and 8 females, 7.8 +/- 3.8 years old). The biopsies were performed within the initial 3 months after the onset of urinary abnormalities in all patients. Twelve patients had crescents (% glomeruli with crescents; 27.5 +/- 20.4%), and the other 7 did not. Renal tissues biopsied from 10 patients with asymptomatic hematuria served as controls for quantitative studies of glomerular leukocyte infiltration. Prominent endocapillary proliferation as well as fibrinoid necrosis were encountered in patients with crescents in contrast to patients without crescents. A positive correlation between crescents and endocapillary proliferation or fibrinoid necrosis was also observed. Significant increases in the number of glomerular CD68+ macrophages, CD45RO+ T cells and NP57+ neutrophils were observed in HSPN patients compared with the controls. When patients with or without crescents were compared, patients with crescents had a greater number of inflammatory cells. Although all kinds of inflammatory cells appeared in the endocapillary proliferative lesion, only CD68+ macrophages and NP57+ neutrophils were present in the fibrinoid necrotizing lesion. In conclusion, the present study demonstrated that necrotizing lesions with capillary rupture may be essential in the process of crescent formation seen in HSPN. Although the mechanism by which capillary wall breaks occur is still unknown, this study indicates that infiltrating macrophages as well as neutrophils may be involved in capillary rupture leading to epithelial crescent formation.
上皮新月体形成与紫癜性肾炎(HSPN)患者的预后密切相关,但关于该疾病新月体形成的机制却知之甚少。在本研究中,我们探讨了肾小球毛细血管内增生、纤维蛋白样坏死和浸润性炎症细胞是否参与新月体形成过程。从19例患者(11例男性,8例女性,年龄7.8±3.8岁)获取肾活检标本。所有患者均在出现尿液异常后的最初3个月内进行活检。12例患者有新月体(有新月体的肾小球百分比;27.5±20.4%),另外7例没有。从10例无症状血尿患者获取的肾组织活检标本用作肾小球白细胞浸润定量研究的对照。与无新月体的患者相比,有新月体的患者出现显著的毛细血管内增生以及纤维蛋白样坏死。新月体与毛细血管内增生或纤维蛋白样坏死之间也观察到正相关。与对照组相比,HSPN患者肾小球CD68+巨噬细胞、CD45RO+T细胞和NP57+中性粒细胞数量显著增加。比较有或无新月体的患者时,有新月体的患者炎症细胞数量更多。尽管各种炎症细胞都出现在毛细血管内增生性病变中,但纤维蛋白样坏死性病变中仅存在CD68+巨噬细胞和NP57+中性粒细胞。总之,本研究表明,伴有毛细血管破裂的坏死性病变可能是HSPN中所见新月体形成过程的关键。虽然毛细血管壁破裂发生的机制尚不清楚,但本研究表明,浸润的巨噬细胞以及中性粒细胞可能参与导致上皮新月体形成的毛细血管破裂。