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目的:探讨糖原合成酶激酶在移植肾组织中的表达及其在慢性移植肾失功发病机制中的意义。方法:收集解放军第181医院2007年01月～2009年12月因蛋白尿或肌酐升高而行肾脏穿刺术的肾移植患者的肾穿标本。其中病理诊断符合慢性移植肾失功的病例有28例,包括男21例,平均年龄(45±10)岁,女7例,平均年龄(42±9)岁,肾穿时间为肾移植术后1年～9年,平均3.5年,血清肌酐(206±122)μmol/L。利用免疫组织化学技术和计算机真彩色图像分析系统(imagepro-plus6.0)半定量检测28例慢性移植肾失功患者移植肾组织中糖原合成酶激酶的表达情况,计算GSK表达的平均面积和平均累计光密度,分析GSK-3β表达水平与移植肾组织炎症细胞浸润、间质纤维化/小管萎缩程度之间的关系。5例正常肾组织作为对照组。结果:慢性移植肾失功患者肾组织中GSK-3β的表达比正常肾组织明显增加,并随肾组织炎症细胞浸润、间质纤维化、小管萎缩程度而递增。结论:糖原合成酶激酶的高表达与移植肾肾组织炎症细胞浸润、间质纤维化/小管萎缩存在正相关关系。
Objective: To investigate the expression of glycogen synthase kinase in renal allograft and its significance in the pathogenesis of chronic graft failure. Methods: We collected renal peritoneoscope specimens from renal transplant patients who underwent renal puncture due to proteinuria or creatinine in the 181st Hospital of PLA from January 2007 to December 2009. Among them, 28 cases were pathologically diagnosed as chronic graft failure, including 21 males, with an average age of (45 ± 10) years and 7 females with an average age of (42 ± 9) years. Renal penetration time was 1 year to 9 years, an average of 3.5 years, serum creatinine (206 ± 122) μmol / L. Immunohistochemistry and computer true color image analysis system (imagepro-plus6.0) semi-quantitative detection of 28 cases of chronic renal allograft failure in renal graft glycogen synthase kinase expression, calculate the average area of GSK expression and The average cumulative optical density was analyzed. The relationship between the expression of GSK-3βand inflammatory cell infiltration and interstitial fibrosis / tubular atrophy in renal allograft was analyzed. 5 cases of normal kidney tissue as a control group. Results: The expression of GSK-3β in renal tissue of patients with chronic graft failure was significantly higher than that in normal renal tissues and increased with the infiltration of inflammatory cells, interstitial fibrosis and tubular atrophy in renal tissues. CONCLUSION: The high expression of glycogen synthase kinase has a positive correlation with inflammatory cell infiltration and interstitial fibrosis / tubular atrophy in renal allograft.