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作 者:达展云[1] 范亚平[1] 沈良兰[2] 施岚[1] 王锋[1] 刘海泉[1]
机构地区:[1]南通大学附属医院肾脏风湿免疫科,江苏南通226001 [2]南通大学第二附属医院肾脏风湿免疫科,江苏南通226001
出 处:《中国现代医学杂志》2009年第15期2381-2385,共5页China Journal of Modern Medicine
基 金:国家自然科学基金(No:30670986);江苏省自然科学基金(No:BK2006059)
摘 要:目的比较足细胞裂孔膜蛋白Nephrin和Podocin在特发性膜性肾病(IMN)及两种常见继发性膜性肾病V型狼疮性肾炎(LN-V)与乙型肝炎病毒相关性膜性肾病(HBV-MN)中表达的差异,探讨Nephrin和Podocin在膜性肾病发病中的作用。方法选取2005年1月~2008年6月行肾穿刺活检确诊的IMN15例、LN-V12例、HBV-MN9例,另取5例正常肾脏组织作对照,收集尿常规、24h尿蛋白定量、肝肾功能、血脂和尿C3等临床检验指标,肾组织标本行间接免疫荧光激光共聚焦显微镜观察各组足细胞裂孔膜蛋白Nephrin和Podocin表达的改变。结果3组病例24h尿蛋白定量、血清白蛋白、血清肌酐和尿C3差异无统计学意义,LN-V组尿红细胞计数高于IMN组,LN-V组及HBV-MN组血清总胆固醇、三酰甘油低于IMN组;间接免疫荧光激光共聚焦显微镜显示3组膜性肾病Nephrin和Podocin表达均较对照组减弱,但以IMN组最为明显,LN-V与HBV-MN两组间无差别。结论足细胞裂孔膜蛋白Nephrin和Podocin在原发性及继发性膜性肾病中表达均减弱,免疫介导的足细胞损伤所致足细胞裂孔膜蛋白减少可能参与了原发性与继发性膜性肾病蛋白尿的发生;但IMN中Nephrin、Podocin表达减弱较继发性膜性肾病更为明显,推测后者蛋白尿的发生还有其他因素参与。[ Objective] To investigate the expression changes of slit diaphragm proteins of glomerular podocyte, such as nephrin and podocin in idiopathic membranous nephropathy (IMN), type V lupus nephritis (LN-V) and hepatitis B virus associated membranous nephropathy (HBV-MN). [Methods] 15 cases with IMN, 12 with LN-V and 9 with HBV-MN were enrolled in the study. 24 hours urine protein excretion, serum albumin, creatinine, triglyceride, total cholesterol, urine C3 and glomerular histopathology were observed respectively. The expressions of nephrin and podoein were determined by indirect immunofluorescent staining. [Results] There were no differences in 24 hours urine protein excretion and the concentrations of serum albumin, ereatinine, urine C3 among 3 groups. Triglyceride and total cholesterol in LN-V and HBV-MN groups were not as high as those in IMN group (P 〈0.05). By indirect immunofluoreseent histochemistry, the expressions of nephrin and podocin were significantly decreased in IMN, LN- V and HBV-MN groups. However, the decreased expression of nephrin and podoein is more obviously in IMN group than those in LN-V and HBV-MN groups. [Conclusions] The expression changes of nephrin and podocin play an important pathogenefic role in IMN, LN-V and HBV-MN. There might be present other mechanisms producing significant proteinuria in secondary MN, like LN-V and HBV-MN.
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