肥大细胞在过敏性紫癜肾炎患儿肾间质纤维化中的作用

目的：探讨肥大细胞（mast cell，MC）在过敏性紫癜肾炎（HSPN）患儿肾间质纤维化的作用及可能机制。方法：以20例HSPN患儿肾活检石蜡切片组织作为研究对象，5例肾肿瘤病人行肾切除的远离肿瘤部位的肾石蜡切片组织作为对照组，应用免疫组化方法对肾组织中的β-类胰蛋白酶（肥大细胞活化的标志物）和转化生长因子-β1（transforming growth factor-β1 , TGF-β1）进行检测，用甲苯胺蓝组织化学法计数组织切片中的MC，并与HSPN患儿肾组织病理积分进行相关分析。结果：①肾组织中MC、β-类胰蛋白酶阳性细胞率、TGF-β1的表达水平积分与对照组之间比较差异有显著性（P<0.05）；②肾组织中MC、β-类胰蛋白酶阳性细胞率及TGF-β1的表达水平积分与肾小球病理积分之间有明显的正相关关系（r =0.940,0.920,0.937，P <0.05）、与肾小管间质病理积分之间有明显的正相关关系（r=0.903,0.859,0.948，P <0.05）、与肾间质纤维化积分存在明显正相关关系（r =0.790,0.766,0.858，P<0.05）；③MC与β-类胰蛋白酶阳性细胞率、MC与TGF-β1表达水平积分、β-类胰蛋白酶阳性细胞率与TGF-β1表达水平积分三者之间存在明显的正相关关系（r＝0.941,0.942,0.897，P<0.05）。结论 MC肾组织浸润与小儿HSPN肾间质纤维化的发生发展密切相关，其可能机制为MC及其分泌的β-类胰蛋白酶、TGF-β1共同参与小儿HSPN肾间质纤维化的发生、发展。［中国当代儿科杂志，2007，9（2）：125-128］

Role of mast cells in the development of renal interstitial fibrosis in children with Henoch-Schonlein purpura nephritis

OBJECTIVE: To investigate the role of mast cells in the development of renal interstitial fibrosis in children with Henoch-Schonlein purpura nephritis (HSPN) and possible mechanisms. METHODS: Paraffin-embedded renal biopsy tissue sections from 20 children with HSPN were examined for the levels of tryptase-beta and transforming growth factor-beta1 (TGF-beta1) by immunohistochemical staining. Mast cells were counted by toluidine blue staining. Masson staining was used to assess the level of renal interstitial fibrosis and renal histopathological scores. Normal renal tissue sections from 5 nephrectomized children for nephroma were used as control group. RESULTS: The percentages of positive tryptase-beta cellsand mast cells and the TGF-beta1 expression in the HSPN group were significantly higher than those in the control group (P < 0.05). The percentages of positive tryptase-beta cells and mast cells and the TGF-beta1 expression in renal tissue were positively correlated with the glomeruli histopathological score (r =0.940, 0.920, 0.937, respectively; P < 0.05) and were also positively correlated with the histopathological score of renal interstitium (r=0.903, 0.859, 0.948, respectively; P < 0.05). The level of renal interstitial fibrosis was positively correlated with the percentages of positive tryptase-beta cells and mast cells and the expression of TGF-beta1 (r =0.790, 0.766, 0.858, respectively; P < 0.05). There was a positive correlation between the percentages of positive tryptase-beta cells and mast cells (r =0.941, P < 0.05), between the percentage of positive tryptase-beta cells and the TGF-beta1 expression (r =0.897, P < 0.05) and between the percentage of positive mast cells and the TGF-beta1 expression (r=0.942, P < 0.05). CONCLUSIONS: Tubulointerstitial mast cell infiltration is associated with the development of renal interstitial fibrosis in children with HSPN. Mast cells together with TGF-beta1 and mast cell-derived tryptase-beta may be involved in the development of the renal interstitial fibrosis in HSPN.