胰肾联合移植治疗肝移植后糖尿病合并肾功能衰竭二例

目的 总结肝移植后再行胰肾联合移植治疗糖尿病合并肾功能衰竭的临床处理经验.方法 2例肝移植受者术前合并有2型糖尿病,分别于肝移植后7年余和4年余发生肾功能衰竭,遂行胰肾联合移植,2例的移植肝功能均正常.采取腹部器官联合快速切取技术整块切取双肾、全胰及十二指肠节段,先行肾移植,再行胰腺移植,供肾移植于左侧髂窝,供胰移植于右侧髂窝,供者的十二指肠与受者的空肠侧侧吻合,供者的十二指肠内置管,通过受者的空肠引流出体外.例1采用抗白细胞介素受体单克隆抗体诱导的四联免疫抑制方案预防排斥反应;例2术中给予抗胸腺细胞球蛋白和甲泼尼龙,术后继续使用2d,采用他克莫司+吗替麦考酚酯+皮质激素预防排斥反应.结果 2例手术过程顺利,术后移植胰腺功能正常,血糖均于术后10d左右恢复正常,无需胰岛素治疗,移植肾功能1周时恢复正常,第2例1周后血清肌酐渐进性升高,经验性抗排斥反应治疗效果不明显,移植肾活组织检查未见明显排斥反应征象,遂将他克莫司替换为西罗莫司,之后受者的肾功能逐渐恢复正常.目前2例受者已分别随访36个月及9个月,移植肝、肾及胰腺功能均正常.结论 肝移植后合并糖尿病、肾功能衰竭时可考虑行胰肾联合移植,但术后免疫反应复杂,需严密监测移植物功能.     

肠道-腔静脉引流的胰肾联合移植术

目的 探讨肠道-下腔静脉引流的胰肾联合移植术的手术操作及临床效果.方法 对3例慢性肾衰竭合并2型糖尿病患者施行肠道-腔静脉引流的胰肾联合移植术,3例均为首次移植,年龄52、58、58岁.每日胰岛素用量20～55 U.供体切取均采用多器官联合切取.热缺血时间8～12 min,供体修整均采用肝总动脉与胃十二指肠动脉端-端吻合以重建十二指肠动脉弓,利用供体髂总静脉延长供体门静脉,切除供体脾脏.以供体髂内动脉与供肾动脉端-端吻合备用.受者手术采用右下腹经腹直肌切口,游离腔静脉下段及右侧髂外动静脉,取动脉延长之供肾,将供肾静脉与受者髂外静脉行端-侧吻合,将供体髂总动脉与受者髂外动脉行端-侧吻合,供体髂外动脉(残端修整成斜面)以动脉夹暂时夹闭备用,十字切开侧腹膜,将供肾埋入,输尿管经腹膜外隧道牵至膀胱底行膀胱输尿管吻合术,胰腺移植采用供体门静脉与受者下腔静脉行端-侧吻合,腹腔干-肠系膜上动脉之腹主动脉袖片与供体髂外动脉残端吻合,开放血流后行供体十二指肠与受体小肠侧侧吻合并关闭十二指肠残端.术后保留胃肠减压,待患者胃肠道功能恢复后拔除.每4 h测血糖、每6 h测血清及胰周引流液淀粉酶1次,每日超声监测胰腺及肾脏血流,生长抑素0.1 mg皮下注射8 h 1次,2周后停用.免疫诱导采用抗胸腺细胞免疫球蛋白减激素方案.结果 3例患者手术过程顺利,手术时间分别为7.5、8.0及10.0 h,术中失血量300～500 ml,仅1例术中输注浓缩红细胞2 U.术后1～3 d内完全停用胰岛素.术后3～7 d内移植肾功能恢复正常.实验室检查SCr分别为86、98及112μmol/L.1例术后10 d出现消化道出血,考虑为肠道吻合口出血;停用抗凝药.给予止血药及输血6 U治疗后1 d出血停止.3例随访2～6个月,无排斥反应发生,空腹及餐后血糖正常.结论 利用供体髂动脉搭桥的方法进行的胰肾同侧联合移植术手术操作简单,创伤较小而且仪使用一侧髂血管,对于左侧髂动脉硬化严重的患者仍可施行该术式.因而扩大了受者的范围;为患者保留一侧髂血管,为今后再次肾移植创造了条件.同时腔静脉引流的胰肾联合移植术使供体门静脉与脾静脉的夹角更符合生理角度,可能减少脾静脉血栓形成的发生率.     

胰肾联合移植的供体切取与修整7例

目的　总结胰肾一期联合移植手术的供体切取和修整方法。方法　采用原位灌注联合切取和体外修整的方法完成7例尸 体供胰、十二指肠和肾的联合切取与修整。结果　7例获取器官的热缺血时间平均3分30秒,联合切取器官时间14分20秒,灌 注液平均用量1050mL。用切取、修整的胰、肾完成了3例胰肾联合移植和9例肾移植,均迅速恢复功能,未出现严重外科并发 症。3例胰肾联合移植术后均完全停用胰岛素,正常饮食,胰肾功能正常存活已分别达34个月、25个月和21个月。结论　供体 切取和修整的质量是胰肾联合移植成功的关键之一,此原位灌注联合切取和体外修整的方法可提供保证。     

同期胰肾联合移植12例报告--德国埃森大学的经验

目的总结同期胰肾联合移植(SPK)术的治疗效果和经验。方法自2002年1月至2003年9月,以SPK术治疗胰岛素依赖型糖尿病(IDDM)合并终末期肾病(ESRD)患者12例。每例受者接受来自同一供者的胰腺和肾脏,移植肾以经典方法植入左侧盆腔,胰腺植于右下腹。1例移植胰腺静脉与受者门静脉系统吻合,11例与体静脉系统吻合。胰腺外分泌引流方法为:3例移植物十二指肠段与受者十二指肠吻合,9例与空肠上段吻合。术前应用甲泼尼龙及抗胸腺细胞球蛋白作为免疫诱导,术后以他克莫司、霉酚酸酯和泼尼松三联抗排斥药物维持。结果术后平均随访时间23个月,受者、移植胰腺和移植肾的存活率分别为100%、91.7%和91.7%。1例再次行SPK术的受者,术后出现了超急性排斥反应,且未能逆转,于术后13d切除移植物;其余11例首次行SPK术的受者中,3例(28.3%)出现急性排斥,均获成功纠治。2例受者术后移植肾功能延迟恢复,行过渡性透析。11例首次行SPK术的移植胰腺术后立即发挥了功能,分别于术后1~5d内停用胰岛素。结论同期胰肾联合移植是胰岛素依赖型糖尿病合并终末期肾病患者的一种安全而有效的治疗方法。     

胰液膀胱引流式胰肾联合移植的远期疗效分析

目的：探讨胰液膀胱引流式胰肾联合移植的远期效果及其影响因素。方法：2001年9月～2006年1月共为14例患者行同种异体胰、十二指肠及肾联合移植术。胰腺移植于右髂窝,门静脉与髂外静脉做端侧吻合,包括腹腔动脉干和肠系膜上动脉的腹主动脉片与髂外动脉做端侧吻合,肾脏同常规肾移植于左侧髂窝。十二指肠与膀胱侧侧吻合。胰液采用膀胱外引流。术后应用他克莫司加霉酚酸酯加泼尼松三联免疫抑制方案。结果：9例患者术后胰肾功能恢复良好,早期无排斥反应发生。随访18～70个月,平均34个月。存活5年以上者4例,4年以上者5例,3年以上者6例,1年以上者9例,胰肾功能良好,血糖正常,均未使用降糖药。1例因超急性排斥反应术后第2天切除移植胰腺,随访至今2年肾功能良好。4例死亡,其中3例死于心血管事件、多器官衰竭,1例因十二指肠瘘死亡。结论：仔细完善的围手术期管理、预防和及时处理并发症、合理应用免疫抑制剂是影响胰肾联合移植患者和移植物长期存活的重要因素。     

胰十二指肠及肾一期联合移植5例报告

目的 进一步总结胰十二指肠肾一期联合移植术的经验。方法 回顾性总结4年来共实行的5例胰十二指肠肾脏一期联合移植术的方法、疗效及并发症的预防和治疗。结果 5例术后移植胰腺和移植肾均发挥了正常功能,术后第1－10d均停用胰岛素,空腹血糖在正常范围。术后并发症的发生仍很常见,部分病人出现了诸如胰周感染,脓肿,十二指肠残瘘,化学性或细菌性膀胱炎,移植胰CMV感染,代谢性酸中毒,肺部感染和急性排斥反应等1个或多个并发症。并发症经处理后大多都能得到控制。5例中有两例已分别存活4年6个月和3年5个月,1例术后3周死于移植肾急性排斥反应多器官衰竭,另2例术后至今已10－11个月仍存活较好。结论 胰十二指肠肾脏一期联合移植对治疗1型糖尿病并发晚期尿毒症具有肯定的临床疗效,较其它移植有许多优点。术后并发症的预防和正确治疗是影响病人长期存活的重要因素。     

快速胰肾联合切取的体会

尽管同期胰肾联合移植的胰腺一年存活率已提高到了 82 % 〔1〕,但此手术仍充满了与技术有关的高并发症〔2〕。切取高质量的胰腺是胰腺移植获得成功的基础。在美国不稳定供体 ,整块切取腹腔脏器 ,也有报道〔3〕。我们都是快速整块切取胰腺和肾脏 ,然后在体外将胰与肾脏分开。从 2 0 0 1年 1月至2 0 0 2年 11月 ,我们胰肾联合切取 32例 ,其中做胰肾联合移植 6例。另外 5 8个肾仅做肾移植 ,移植后胰肾功能良好 ,仅 1例发生胰腺和肾功能延迟恢复。现将我们联合切取胰肾的方法介绍如下。资料与方法供体取仰卧位 ,常规消毒铺单。取腹部“十”字型…     

接受同一供体肝肾联合移植与肾移植的临床研究

目的探讨肝肾联合移植肝脏对肾脏的保护作用。方法我院移植中心2002年5月至2006年9月间共进行8例肝肾联合移植手术，对此8例患者及接受同一供体对侧供肾8例肾移植患者及移植物存活率、排斥反应发生率进行分析。结果肝肾联合移植患者及移植物存活率为100％，无可证实排斥反应发生。术后8例患者移植肝功能迅速恢复正常，7例移植肾功能迅速恢复正常，1例移植肾发生急性肾小管坏死，于术后第52天肾功能恢复正常。对应8例单纯肾移植患者，发生急性排斥反应1例，予甲基强的松龙冲击治疗及应用抗人T淋巴细胞免疫球蛋白（anti-thymocyte globulin，ATG）后，于术后50d移植肾功能恢复正常，余7例患者恢复良好，至末次随访肾功能均正常。结论肝肾联合移植肝脏对肾脏有一定的保护作用。     

胰肾联合移植的外科技术探讨

目的 探讨胰液空肠引流式胰肾联合移植的外科技巧和临床应用.方法 中山大学附属第一医院2005年1月-2009年6月共施行了10例胰肾同期联合移植术(SPK),供体胰、十二指肠和肾均采用腹部多器官联合切取方式获得,经腹主动脉、肠系膜上静脉对胰腺及十二指肠同时快速灌注降温.移植胰的外分泌采用胰十二指肠一空肠内引流吻合方式.术后早期均以抗CD25单克隆抗体进行免疫诱导治疗,采用他克莫司、霉酚酸酯及皮质激素预防排斥反应.结果 10例移植手术均获得成功.供体胰十二指肠和肾的热缺血时间为(5.9±2.6)min;移植肾平均冷缺血时间为(5.2±2.2)h,移植胰平均冷缺血时间为(9.3±3.6)h.术后3例出现移植胰伤口感染,经治疗后3～12周愈合.2例出现胰十二指肠一空肠吻合口出血,均经保守治疗止血而治愈.未发生与胰液引流相关的外科并发症.1年内3例发生了急性排斥反应,2例经激素冲击和抗淋巴细胞球蛋白治疗而被逆转;1例顽固性急排患者术后39 d在持续肾脏替代治疗过程中并发脑血管意外死亡.其余9例均痊愈,随访6～12个月,完全停用胰岛素.结论 获取质量良好的供体器官及合理血管整形,是保证胰肾联合移植成功的前提;改进的胰液空肠外分泌引流术式的方法是可靠的.     

胰肾一期联合移植

目的 总结胰肾联合移植治疗糖尿病并发晚期肾功能不全病人的疗效,并探讨分析术后并发症防治经验。方法 对５例糖尿病并发现期肾小功能不全者采用胰十二指肠肾一期联合移植。免疫抑掉方案采用激素,ＣｓＡ及硫唑嘌呤或激素,ＣｓＡ及骁悉三联用药。结果 联合移植后５例胰肾均发挥正常功能,病人均立即停用胰岛素,１例术后发生移植肾急性排斥以应,死于多器官功能衰竭,余４例分别发生胰周脓肿,急性胰腺炎,十二指肠瘘,血尿等并     

Impact of Simultaneous Kidney–Pancreas Transplant and Timing of Transplant on Kidney Allograft Survival

Since 1988 over 10 000 simultaneous cadaveric pancreas-kidney transplants (SPK) have been performed in the United States among patients with end-stage renal disease due to Type 1 diabetes (T1DM). The two aims of this study were to assess the impact on kidney allograft survival of (i) SPK versus transplantation of a kidney alone (KA), and (ii) SPK prior to versus after initiation of chronic dialysis. This retrospective, non-concurrent cohort study examined registry data collected from 8323 patients waitlisted in the United States for an SPK and transplanted with either an SPK or a KA during January 1, 1990 - October 31, 2002. SPK recipients had an adjusted hazard ratio for kidney allograft loss of 0.63 (95% CI: 0.51-0.77, p < 0.001) compared to transplantation without pancreas allograft. SPK recipients who received their allografts prior to beginning chronic dialysis had a lower rate of kidney allograft loss than SPK recipients who received their transplant after initiation of chronic dialysis (adjusted hazard rates (HR) = 0.83, 95% CI: 0.69-0.99, p = 0.042). Simultaneous transplantation of pancreas-kidney compared to kidney transplantation alone and SPK prior to the initiation of chronic dialysis compared to SPK after initiation of dialysis were both associated with longer kidney allograft survival.     

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。     

A three-year experience with serum anodal trypsinogen as a biochemical marker for rejection in pancreatic allografts. False positives, tissue biopsy, comparison with other markers, and diagnostic strategies.

Serum values of immunoreactive anodal trypsinogen (sAT) have been claimed to correlate well with rejection occurring in pancreatic allografts. We have studied the behavior of sAT in serial serum samples obtained from 39 type I diabetics undergoing whole-organ pancreas transplantation during the past 3 years. Patients had either received a pancreatic allograft simultaneously with a transplanted kidney (SPK, n = 33) or after a previous kidney transplant (pancreas after kidney [PAK] n = 6). The behavior of sAT was studied in relation to the clinical diagnosis of rejection. Graft amylase output for all 39 patients and serum creatinine for the 33 SPK recipients were also studied. Tissue biopsies were obtained from 11 patients with elevated sAT values and a presumptive diagnosis of rejection. Nine of these patients had SPK grafts and simultaneously elevated creatinine values. Tissue was obtained from the simultaneously transplanted kidney; all specimens revealed rejection. Two of the 11 patients had PAK allografts. Biopsies performed on the graft duodenum were consistent with acute rejection. Three additional patients with unchanged sAT values had biopsies for other reasons; these biopsies failed to demonstrate signs of acute rejection. Thus graft biopsy correlated exactly with sAT behavior in every case in which rejection was suspected. Five patients had elevations of sAT not associated with rejection: one resulted from direct trauma, two had outlet obstruction, and two had clinical diagnoses of graft pancreatitis. The sAT was more sensitive and specific than GAO and as sensitive as creatinine for SPK recipients. These studies confirm that sAT is a reliable, graft-specific biochemical marker for the early diagnosis of pancreatic rejection. The use of sAT should allow for the proper timing of graft biopsies and the judicious use of immunosuppressive agents, which will result in increased allograft survival for PAK and pancreas-alone allografts.     

Randomized, prospective trial of mycophenolate mofetil versus azathioprine for prevention of acute renal allograft rejection after simultaneous kidney-pancreas transplantation

BACKGROUND: In simultaneous kidney-pancreas (SPK) transplantation, manifestations of renal allograft rejection typically become evident before those of pancreatic rejection. This study compared mycophenolate mofetil (MMF) and azathioprine (AZA) in prevention of renal rejection after primary SPK transplantation. METHODS: In an open-label, randomized, multicenter study, patients received MMF 1.5 g twice daily (n=74) or AZA 1-3 mg/kg daily (n=76) for 1 year after transplantation. The incidence of rejection was assessed at 6 months. Adverse events were tracked through 1 year. Survival data are reported through 2 years. RESULTS: At 6 months, efficacy results for MMF vs. AZA patients, respectively, were the following: rejection (27% vs. 39%); rejection or death (34% vs. 42%); rejection, graft loss, death, or premature withdrawal (i.e., treatment failure; 41% vs. 55%). Six-month efficacy trends favored MMF, and time to rejection or treatment failure was significantly longer when compared with AZA (P=0.049). One-year efficacy results for MMF vs. AZA patients, respectively, were the following: treatment of renal rejection (35% vs. 47%); renal allograft loss or death (9% vs. 12%); pancreas allograft loss or death (15% vs. 14%). Five MMF patients (7%) and four (5%) in the AZA group died. More MMF than AZA patients developed opportunistic infections (54% vs. 38%), but the pathogens did not differ. CONCLUSIONS: Trends for most efficacy parameters favored MMF over AZA, and time to renal allograft rejection or treatment failure was statistically significantly longer for MMF. The use of MMF in the treatment of SPK recipients is a useful advance.     

Single-shot antithymocyte globuline and daclizumab induction in simultaneous pancreas and kidney transplant recipient: three-year results

Since 1996, preoperative single-shot dose antithymocyte globuline (ATG) with prednisolone (PRD), mycophenolate mofetile (MMF), and tacrolimus (TAC) is the favorite induction therapy in our center. In a series of 25 first simultaneous pancreas and kidney transplant (SPK) recipients, 5 doses of daclizumab were administered in addition to standard induction. Here we present our 3-year experience. Immunosuppression was started prior to reperfusion consisting of daclizumab (1 mg/kg body weight [bw]), ATG (4-6 mg/kg bw) and 250 mg PRD. After surgery, PRD was reduced gradually, TAC trough levels were between 8-15 ng/mL, MMF was given twice daily (2-3 g/d) as well as 4 further doses dacilzumab every 14 days. After 3 years, patient, pancreas, and kidney graft survival rates are 100%, 84%, and 92%, respectively. Four pancreas grafts were lost (chronic allograft dysfunction, n = 2; recurrent abdominal infection, n = 1; acute rejection [AR] without treatment, n = 1). Both patients suffering from severe infection and untreated AR lost their kidney graft too. During the first 3 months after SPK, 3 AR episodes were observed in 2 patients (8%). After a 3-year period, 8 AR episodes occurred in 7 recipients (28%). AR was treated using PRD (n = 5) or ATG (n = 1). In 1 case, immunosuppression was switched from TAC to sirolimus successfully. Overall, 8 AR episodes occurred in 7 patients (28%) during the first 3 years after SPK. One severe infection led to graft lost 13 months after SPK. In this series, the combination of ATG and daclizumab prevented AR episodes, successfully providing considerable 3-year survival rates.     

Risk of adverse post-transplant events after kidney allograft transplantation as predicted by CTLA-4 +49 and TNF-alpha -308 single nucleotide polymorphisms: a preliminary study

Genetic differences between donor and recipient HLA haplotypes are of major importance for transplant rejection. Other genetic variations occurring in genes encoding cytokines and costimulatory molecules also appear to exert an influence on the manner the host immune system recognizes the allograft. The aims of this work were: 1) to study selected single nucleotide polymorphisms (SNPs) at the loci encoding the T-cell regulatory molecule CTLA-4 (CD152), and the cytokines interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-beta1 in a sample of healthy volunteers and a group of kidney-transplanted patients; and 2) to investigate whether an association exists between any of the SNPs studied and acute or chronic rejection, or non-responsiveness to steroid treatment during episodes of acute rejection (AR) after kidney allograft transplantation. When healthy volunteers were compared with transplanted patients, no significant differences were found in the distribution of genetic frequencies for any of the SNPs analyzed. However, in transplanted patients who received a kidney from a living related donor (KdTxL), a statistically significant association was found between carrying the CTLA-4 +49 A/A genotype and protection from experiencing acute rejection. No such association was found in the group of transplanted patients who received a kidney from a cadaveric non-related donor (KdTxCad). In both, KdTxL and KdTxCad patients, responsiveness to steroid treatment during acute rejection was also in association with the CTLA-4 (+49A/G) SNP. The CTLA-4 +49G allele was found at a very low frequency among steroid-resistant compared with steroid-sensitive patients. Finally, a statistically significant association was found between the presence of the TNF-alpha -308A allele and protection to suffer from chronic rejection. The genetic differences found may serve as risk predictors of adverse post-transplant events.     

肝胰肾联合移植的免疫抑制治疗

目的 介绍1例存活超过1年的肝胰肾联合移植患者术后免疫抑制治疗方法。方法对1例肝炎后肝硬化合并尿毒症、I型糖尿病、慢性胰腺炎患者施行原位背驮式肝、胰液空肠引流式胰、十二指肠及肾一期联合移植，采用二剂巴利昔单抗（舒莱）诱导，抗胸腺细胞球蛋白（ATG）、他克莫司（FK506）、吗替麦考酚酯（MMF）、泼尼松四联维持治疗。结果 术后移植肝脏及胰腺功能1周内逐渐恢复；肾功能延迟恢复，于术后第16天因消化道大出血致肾脏血流下降，切除移植肾脏，于原移植部位进行第2次肾移植，术后第3天肾功能恢复正常，未发生排斥反应。患者已健康存活超过1年，移植肝、胰、肾功能良好，生活自理。结论 肝胰肾联合移植术前后采用二剂舒莱诱导，同时用ATG、FK506、MMF及泼尼松作为免疫维持治疗安全有效，用药期间进行移植物功能、血药浓度及T细胞亚群（CD4^＋，CD4^＋）监测是防治排斥反应、感染及药物中毒的有效手段。     

“二袖套法”大鼠原位肝移植的技术改进

目的 探讨大鼠原位肝移植(OLT)模型的技术改进方法,并观察移植后的排斥反应。方法 将“二袖套法”大鼠肝移植技术进行了改进;并行SD→SD,SD→Wistar大鼠肝移植各30例,观察术后排斥情况。结果 全组肝移植手术无肝期约为15min。大鼠无手术死亡。SD-SD大鼠肝移植后3周内存活率为97％;SD→Wistar大鼠肝移植后8～15d死亡,组织病理学证实存在不同程度的排斥反应。结论 采用该改良大鼠肝移植方法可明显缩短手术时间,降低术后并发症,提高移植大鼠的术后生存率。SD-Wistar大鼠的肝移植可作为较理想的研究肝移植排斥反应的动物模型。     

ATG-F与OKT3在肾移植术后急性排斥反应中的应用研究

目的 探讨应用注射用兔抗人T淋巴细胞多克隆抗体(ATG-F)及注射用抗人T细胞CD3鼠单克隆抗体(OKT3)治疗肾移植术后急性排斥反应的效果、安全性和副反应等.方法 本中心施行同种异体肾移植术后对于激素冲击治疗不敏感的急性排斥患者51例,分为两组,分别给予多克隆抗体ATG-F和单克隆抗体OKT3治疗,并对治疗效果、安全性和药物的副反应等进行统计学分析.结果 ATG-F治疗28例,排斥逆转26例,治愈率89.3％;OKT3抗组23例,排斥逆转16例,治愈率69.6％.两组结果间有显著性差异(P＜0.05).结论 OKT3和ATG-F同为抗淋巴细胞的抗体,但其针对难治性急性排斥反应的治疗效果,存在明显差异.ATG-F临床效果肯定,并且用量灵活,副作用小.OKT3治疗效果一般,则具有术后感染发生率增加、白细胞减少等并发症.     

Pancreas-after-kidney transplantation: an increasingly attractive alternative to simultaneous pancreas-kidney transplantation

BACKGROUND: Historically, the clinical acceptability of pancreas-after-kidney (PAK) transplantation has been hampered by relatively high acute rejection rates and lower pancreas graft survival rates when compared with the more commonly performed simultaneous pancreas-kidney (SPK) transplantation. The purpose of this study was to compare PAK transplantation to SPK transplantation in the Thymoglobulin induction era. METHODS: The authors reviewed all bladder-drained PAK (n=47) transplants receiving rabbit antithymocyte globulin induction from June 1998 to June 2002 and compared them with SPK (n=25) transplants during the same time period at their institution. The authors retrospectively studied data on demographics, patient survival, graft (pancreas and kidney) survival, complications, and biopsy-proven rejection episodes. RESULTS: The actuarial 1-year patient survival was 93% for the PAK group versus 100% for the SPK group (P =not significant [NS]). The actuarial 1-year pancreas graft survival was 87% for the PAK group versus 92% for the SPK group (P =NS). Waiting time for PAK was significantly shorter than for SPK (6.3 +/- 5.2 vs. 16.2 + -13.7 months, P <0.05). Clinical acute rejection rates were similar in the two groups (4.3% for PAK vs. 4.0% for SPK). PAK recipients demonstrated a greater decline in renal function after transplantation compared with SPK. A multivariate analysis failed to elucidate the cause. CONCLUSIONS: Newer immunosuppressive regimens allow PAK transplant patients to achieve immunologic outcomes similar to SPK transplant patients. Although the shorter waiting time and the ability to use living-donor kidneys make PAK an increasingly attractive alternative to SPK transplantation, its effect on renal allograft function deserves further attention.