肝肾联合移植的单中心经验总结

目的 分析单中心肝肾联合移植(SLKT)的治疗效果.方法 1999-2010年间共实施SLKT 21例,患者的原发疾病分别为多囊病11例,病毒性肝炎后肝硬化合并肝肾综合征5例,慢性肾炎肾功能衰竭合并肝硬化2例,肾移植术后移植肾功能丧失合并肝硬化2例,肝炎后肝硬化合并糖尿病肾病1例.统计患者的资料,与同期同中心"中国肝移植注册网站"收录的肝炎后肝硬化行肝移植的133例(LT组)和"中国肾移植科学登记系统"收录的尸体肾移植609例(KT组)进行对比,分析各组受者术前状态和预后的差异.结果 SLKT组术前终末期肝病模型(MELD)评分为21.3±5.5,血肌酐为(516.0±329.9)mmol/L;LT组术前MELD评分为20.6±9.9,血肌酐为(111.4±138.1)mmol/L,与SLKT组相比较,血肌酐的差异有统计学意义(P＜0.01).SLKT组中,3例分别于术后2周、半年和5年因感染而死亡,1例因多器官功能衰竭而死亡,1例于术后5年自行停药,因排斥反应而死亡.SLKT组术后1年内移植肾急性排斥反应的发生率为零,KT组为6 %(P＞0.05).术后SLKT组移植肾功能延迟恢复的发生率为9.5 %,KT组为17.3 %(P＞0.05).SLKT组术后1、3和5年的受者存活率分别为87.7 %、67.8 %和67.8 %,LT组分别为84.2 %、73.5 %和69.4 %(P＞0.05).结论 SLKT是终末期肝、肾疾病的有效、安全的治疗方法.

Abstract：

Objective To analyze the curative effect of simultaneous liver and kidney transplantation (SLKT) for patients with end-stage liver and kidney diseases and liver cirrhosis patients with hepatorenal syndrome.Methods All SLKTs (n=21) performed at our center from January 1999 to December 2010 were reviewed and SLKT outcomes were compared with those of kidney transplantation (KT) (n=609) and liver transplantation (LT) (n=133) performed during the same period.Results There were 3 deaths due to infection 2 weeks, 6 months and 5 years respectively after operation. One patient died due to multiple organ dysfunction syndrome 2 weeks after operation. One patient was dead 5 years after operation because of rejection. MELD level between SLKT and LT had no significant difference, but serum creatinine in SLKT group was significantly higher than in LT group (516.0±329.9 vs 111.4±138.1 mmol/L, P<0.01). The 1-year acute kidney rejection rate and rate of delayed graft function (DGF) of the kidney had no significant difference between SLKT group (0 vs 9.5 %) and KT group (6 % vs 17.3 %). There was no significant difference in one-, 3- and 5-year patient survival rate between SLKT group (87.7 %, 67.8 % and 67.8 %) and LT group (84.2 %, 73.5 % and 69.4 %).Conclusion SLKT is a safe and effective treatment for end-stage liver and kidney diseases.     

结缔组织生长因子诱导人肾小管上皮细胞向间充质细胞转化的实验研究

Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role.     

结缔组织生长因子诱导人肾小管上皮细胞向间充质细胞转化的实验研究

Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role.     

结缔组织生长因子诱导人肾小管上皮细胞向间充质细胞转化的实验研究

Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role.     

肝癌肝移植后肿瘤复发的原因与治疗

肝癌是否适宜肝移植治疗历来就有争论 ,但就肝细胞肝癌同时伴有肝硬化 ,肝功能较差的患者而言 ,肝移植似乎是惟一的既可以去除肝癌病变 ,又可以去除肝硬化 ,恢复肝功能的治疗方案。近年来随着肝癌肝移植病例的增加及术后随访时间的延长 ,人们意识到移植后肝癌的复发问题是导致患者远期生存率低的主要原因 ,因此认识肝癌复发原因 ,严格掌握肝移植适应证 ,明确肝癌复发的治疗方案是相当重要的。一、原因导致肝癌复发的原因有多种 ,主要包括肝癌肝移植适应证的选择 ,手术术式及手术操作 ,术后免疫抑制治疗等。1.肝癌肝移植适应证选择过宽 :从肿…     

胰液空肠引流术式胰肾联合移植(附10例报告)

总结10例胰液空肠引流(ED)术式胰肾一期联合移植(SPK)的外科技术和治疗胰岛素依赖型糖尿病(IDDM)合并尿毒症的效果。方法2000年6月至2003年7月间完成改进的ED术式SPK10例,不做Roux-en-Y吻合。免疫抑制治疗术后早期采用四联诱导治疗(FK506／CsA MMF 皮质激素 ALG或抗CD25单抗),以后改为三联维持。结果10例手术均获得成功,移植肾功能即刻恢复,除1例移植胰功能延迟恢复外．余9例术后1周内血糖降至正常水平,完全停用外源性胰岛素。1例术后6月带正常移植物功能死于心肌梗塞,4例存活已超过1年;发生急性排斥反应4例次。除1例难治性排斥未能逆转行再次肾移植外．余3例经激素冲击或()KT3治疗均获好转。并发症情况：出现腹腔感染与切口感染各2例,肾周血肿1例,分别经手术探查或引流换药治疗后愈合。结论改进的ED术式胰肾联合移植安全、简单,无严重外科并发症,是值得推广的治疗IDDM合并尿毒症的理想方法。     

腺病毒介导反义细胞外信号调节蛋白激酶2基因转染可延缓移植肾慢性纤维化进程

严重制约肾移植受者长期存活的重要因素是慢性移植。肾纤维化。慢性移植肾纤维化由免疫学和非免疫学因素引起,临床上一般通过调整免疫抑制方案和其他辅助方法予以治疗,目前还没有直接对移植肾纤维化起作用的药物或治疗方案。我们的研究试图寻找可以保护移植物,阻止或延缓移植肾纤维化的方法和相应的治疗靶点。     

抑制NF-κB活性诱导同种异体小鼠心脏移植耐受的早期作用

目的 研究调节性T细胞(Tr)和Th17细胞在特异性NF-κB抑制诱导同种异体小鼠心脏移植耐受的早期作用机制.方法 以BALB/c小鼠为供体,C57BL/6小鼠(对照组)和IκBα△N-Tg小鼠(实验组)分别作为受体建立同种异体腹部异位心脏移植模型;流式细胞术分别检测两组受鼠脾脏内Tr在移植前以及移植术后7 d、30 d和100 d的变化规律,以及Th17细胞在移植术后5 d时的变化;Western blot检测两组心脏移植物内IL-17在移植后3 d和5 d的表达.结果 实验组心脏移植物存活时间均大于100 d,HE染色未见心脏移植物内有明显淋巴细胞浸润;实验组Tr比例在移植后7 d和30 d时明显升高(21.23±3.95,23.17±4.11 vs 11.64±1.96,P0.05),而对照组Tr在移植前后则无明显变化;与对照组相比,实验组Th17细胞及移植物内IL-17表达在移植术后5 d时均明显下降.结论 特异性受体T细胞NF-κB功能缺陷可以打破受体内Tr/Th17细胞平衡,在移植术后早期促进T细胞向Tr分化而抑制向Th17细胞分化,从而阻止急性排斥反应发生,诱导耐受.