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目的探讨肾间质肥大细胞(MC)浸润在乙型肝炎病毒相关性IgA肾病(HBV-IgAN)及原发性IgA肾病(pIgAN)进展中的作用。方法以2008年2月至2011年7月在南京军区福州总医院住院并经肾活检确诊为HBVIgAN和pIgAN患者各30例作为研究对象,6例正常肾组织为对照组。采用免疫组织化学法检测肾间质类胰蛋白酶阳性MC浸润和单核细胞趋化因子(MCP)-1的表达情况,分析其与临床病理指标的关系。结果与对照组相比,pIgANⅡ级肾间质MC浸润数目显著增加(P<0.05),而HBV-IgANⅡ级无明显变化。两组肾间质MC浸润数目随病理分级及肾小管间质损害程度的加重而增加(P<0.05),同时与MCP-1表达水平、肾小管萎缩、间质纤维化、间质炎细胞及血肌酐水平均呈显著正相关(P<0.05)。结论肾间质MC浸润可能通过自分泌MCP-1以介导肾小管间质损害,进而参与HBV-IgAN和pIgAN进展。
Objective To investigate the role of interstitial mast cells (MC) infiltration in the progress of hepatitis B virus-associated IgA nephropathy (HBV-IgAN) and primary IgA nephropathy (pIgAN). Methods From February 2008 to July 2011 in Fuzhou General Hospital of Nanjing Military Region, 30 cases of HBVIgAN and pIgAN were diagnosed by renal biopsy as study object, and 6 cases of normal kidney tissue as control group. Immunohistochemistry was used to detect the expression of renal interstitial tryptase-positive MC infiltration and monocyte chemotactic factor (MCP-1), and its relationship with clinicopathological parameters was analyzed. Results Compared with the control group, the number of MCI in pIgAN Ⅱ grade renal interstitium was significantly increased (P <0.05), while the level of HBV-IgAN Ⅱ did not change significantly. The number of interstitial MC infiltration in both groups increased with the severity of pathological grading and tubulointerstitial damage (P <0.05), and the expression of MCP-1, tubular atrophy, interstitial fibrosis, interstitial inflammatory cells and Serum creatinine showed a significant positive correlation (P <0.05). Conclusion MC infiltration of renal interstitium may mediate tubulointerstitial damage by autocrine MCP-1, and then participate in the progress of HBV-IgAN and pIgAN.