胰肾联合移植后的免疫抑制治疗

背景：胰肾联合移植已经被公认为是糖尿病（包括1型和2型）合并终末期尿毒症的有效治疗手段,由于胰腺为高免疫原性器官,合理的免疫抑制治疗是保证胰腺移植成功的关键。目的：探讨胰肾一期联合移植后免疫抑制药物的合理应用。方法：纳入2005-01/2009-06在中山大学附属第一医院器官移植中心完成胰肾一期联合移植的患者9例,其中男5例,女4例,胰液引流均采用空肠引流方式。术后采用白细胞介素2单克隆抗体诱导的四联免疫抑制方案：白细胞介素2单克隆抗体＋他克莫司＋麦考酚酸＋激素,并逐渐过渡至单用他克莫司维持治疗。回顾性分析以上9例患者围手术期及长期随访情况。结果与结论：胰肾一期联合移植后,除1例早期死亡外,其余8例患者移植后1周内肌酐降至正常水平,移植后停用胰岛素时间为（11.5±3.5）d,空腹血糖恢复至正常时间为（15.4±6.3）d。8例患者随访4～50个月期间,共有4例发生移植肾急性排斥,其中1例在接受床边血液透析过程中并发心脑血管意外后家属放弃治疗,其余3例患者经抗胸腺细胞球蛋白或激素冲击治疗后移植肾功能均逆转恢复,随访过程中未发现移植胰腺排斥。说明胰肾联合移植是治疗糖尿病合并终末期糖尿病肾病的有效方法,术后早期采用白细胞介素2单克隆抗体诱导的四联免疫抑制方案并逐渐过渡至单用他克莫司维持治疗是安全的。     

胰液膀胱引流式胰肾联合移植长期存活15例随访

背景:胰肾联合移植是治疗1型糖尿病合并终末期肾病的首选疗法,但由于移植风险高,并发症多,国内开展并不广泛.目的:总结胰液膀胱引流式胰肾联合移植长期存活的临床经验,观察其远期效果并分析影响因素.方法:对15例患者行胰液膀胱引流式胰肾联合移植,均采用心脏死亡的供体.HLA配型平均为2.13.均选择胰液膀胱引流式和体循环回流血管吻合方式,免疫抑制剂方案均用他克莫司,霉酚酸酯和泼尼松治疗.观察移植后患者移植物肾功能、血糖、淀粉酶等及并发症.结果与结论:最短随访8.5个月,最长随访105.5个月,平均住院时间为37.7 (13～82) d.移植后13例患者胰腺功能恢复,2例于移植后即切除移植胰腺.移植后除1例患者肾脏功能延迟恢复外,其余患者肾脏功能立即恢复.2例患者因慢性排斥反应丢失移植胰腺和移植肾.移植后主要并发症为排斥反应,返流性胰腺炎和血栓形成.提示胰肾联合移植是治疗终末期糖尿病并发肾功能衰竭的一种安全而有效地治疗方法,其远期效果理想,完善的围移植期管理、预防和及时处理并发症、合理应用免疫抑制剂是影响患者和移植物长期存活的重要因素.     

多器官联合移植3例报道

目的:探讨肝肾及胰肾联合移植术的可行性.方法:2例肝炎后肝硬化合并尿毒症患者,分别实施肝肾分期联合移植及肝肾同期联合移植术;1例糖尿病合并尿毒症患者行胰液空肠引流式胰、十二指肠及肾一期联合移植术.术后均采用他克莫司+吗替麦考酚酯+皮质类固醇激素的3联免疫抑制治疗方案,并观察其临床疗效.结果:2例肝肾联合移植患孝术后恢复良好,转氨酶、尿素氮和肌酐恢复正常;胰肾联合移植患者术后停用外源性胰岛素,血糖、C-肽及肾功能恢复正常.随访18～42个月移植器官功能良好.结论:联合脏器移植是治疗多器官功能衰竭的有效手段,能有效提高患者生活质量.     

胰肾联合移植5例分析

背景:胰肾联合是治疗糖尿病合并终末期肾病的最有效方法.但这些患者由于长期糖尿病史,心血管系统疾病相对较复杂,且手术涉及胃肠道,并应用大剂量的免疫抑制约物,移植前准备和移植后处理是胰肾联合移植成功的重要保障.目的:对胰肾联合移植的免疫抑制用药、凝血药物应用、围手术期以及移植后管理注意事项等进行多方面讨论,为胰肾联合移植提供一些临床经验.方法:回顾性分析2003/2008解放军第三○九医院泌尿外科进行胰肾联合移植5例患者的临床资料,总结免疫抑制剂、抗凝药物的应用及围手术期临床监测重点等治疗经验.结果与结论:5例患者均为男性,平均年龄43岁,均为1型糖尿病合并终末期肾病,移植前胰岛素用量为1.5～2.4U,(kg·d),其中1例合并糖尿病视网膜病变,多次眼底出血;2例合并明显冠状动脉粥样硬化性心脏病,移植前心脏射血分数分别为52%和50%.移植胰腺外分泌液均经肠道引流.3例恢复顺利,肾功和血糖均恢复正常.其中1例于移植后第7天出现排斥反应,激素冲击后肾功能恢复;1例移植后出现移植十二指肠急性排斥反应,肠瘘,最终移植胰腺切除,但移植肾脏保留;2例恢复顺利无并发症发生;1例移植后消化道出血,多器官衰竭死亡.胰肾联合移植是治疗糖尿病合并终末肾病的最有效方式.移植胰腺外分泌经膀胱引流由于并发症较多,已被经肠道引流取代.移植肾功能的恢复足胰肾联合移植成功的关键.移植后早期他克莫司可不必急于口服,可待血肌酐恢复到300 pmol/L.时再考虑应用.凝血药物的应用是移植胰腺功能恢复的重要因素之一,空肠造瘘是围手术期预防肠液向移植胰腺返流的重要治疗措施,且移植后随访期建议应用通便药物,预防便秘发生,减少肠液返流引起的急性胰腺炎的发生.     

胰液膀胱引流式胰肾联合移植长期存活15例随访

背景：胰肾联合移植是治疗1型糖尿病合并终末期肾病的首选疗法,但由于移植风险高,并发症多,国内开展并不广泛。目的：总结胰液膀胱引流式胰肾联合移植长期存活的临床经验,观察其远期效果并分析影响因素。方法：对15例患者行胰液膀胱引流式胰肾联合移植,均采用心脏死亡的供体。HLA配型平均为2.13。均选择胰液膀胱引流式和体循环回流血管吻合方式,免疫抑制剂方案均用他克莫司,霉酚酸酯和泼尼松治疗。观察移植后患者移植物肾功能、血糖、淀粉酶等及并发症。结果与结论：最短随访8.5个月,最长随访105.5个月,平均住院时间为37.7（13～82）d。移植后13例患者胰腺功能恢复,2例于移植后即切除移植胰腺。移植后除1例患者肾脏功能延迟恢复外,其余患者肾脏功能立即恢复。2例患者因慢性排斥反应丢失移植胰腺和移植肾。移植后主要并发症为排斥反应,返流性胰腺炎和血栓形成。提示胰肾联合移植是治疗终末期糖尿病并发肾功能衰竭的一种安全而有效地治疗方法,其远期效果理想,完善的围移植期管理、预防和及时处理并发症、合理应用免疫抑制剂是影响患者和移植物长期存活的重要因素。     

Genistein联合小剂量他克莫司在胰腺移植排斥反应中的作用

背景:有实验表明CXCR3拮抗剂Genistein可减轻胰腺移植大鼠的急性排斥反应。目的:观察Genistein联合小剂量他克莫司在胰腺移植抗排斥反应中的作用。方法:以Wistar大鼠为供体,SD大鼠为受体,建立胰腺移植模型,随机分成5组:对照组(未进行药物治疗)、大剂量他克莫司组、小剂量他克莫司组、Genistein组、Genistein+小剂量他克莫司组。术后第7天行病理学,肝肾功能,血清中CD3+、CD4+、CD8+T淋巴细胞、干扰素γ、白细胞介素2浓度检测。结果与结论:与对照组、小剂量他克莫司组、Genistein组比较,Genistein+小剂量他克莫司组移植胰腺组织损伤减轻,淋巴细胞浸润减少,急性排斥反应减轻,血清CD3+、CD4+、CD8+T淋巴细胞明显减少,干扰素γ、白细胞介素2水平降低(P<0.05);并且避免了大剂量他克莫司对肝肾功能的损害。说明Genistein联合小剂量他克莫司能有效减轻胰腺移植急性排斥反应而不增加肝肾毒性。     

多器官联合移植3例报道

目的：探讨肝肾及胰肾联合移植术的可行性。方法：2例肝炎后肝硬化合并尿毒症患者,分别实施肝肾分期联合移植及肝肾同期联合移植术;1例糖尿病合并尿毒症患者行胰液空肠引流式胰、十二指肠及肾一期联合移植术。术后均采用他克莫司＋吗替麦考酚酯＋皮质类固醇激素的3联免疫抑制治疗方案,并观察其临床疗效。结果：2例肝肾联合移植患者术后恢复良好,转氨酶、尿素氮和肌酐恢复正常;胰肾联合移植患者术后停用外源性胰岛素,血糖、C-肽及肾功能恢复正常。随访18～42个月移植器官功能良好。结论：联合脏器移植是治疗多器官功能衰竭的有效手段,能有效提高患者生活质量。     

Genistein联合小剂量他克莫司在胰腺移植排斥反应中的作用

背景：有实验表明CXCR3拮抗剂Genistein可减轻胰腺移植大鼠的急性排斥反应。目的：观察Genistein联合小剂量他克莫司在胰腺移植抗排斥反应中的作用。方法：以Wistar大鼠为供体,SD大鼠为受体,建立胰腺移植模型,随机分成5组：对照组（未进行药物治疗）、大剂量他克莫司组、小剂量他克莫司组、Genistein组、Genistein＋小剂量他克莫司组。术后第7天行病理学,肝肾功能,血清中CD3＋、CD4＋、CD8＋T淋巴细胞、干扰素γ、白细胞介素2浓度检测。结果与结论：与对照组、小剂量他克莫司组、Genistein组比较,Genistein＋小剂量他克莫司组移植胰腺组织损伤减轻,淋巴细胞浸润减少,急性排斥反应减轻,血清CD3＋、CD4＋、CD8＋T淋巴细胞明显减少,干扰素γ、白细胞介素2水平降低（P〈0.05）;并且避免了大剂量他克莫司对肝肾功能的损害。说明Genistein联合小剂量他克莫司能有效减轻胰腺移植急性排斥反应而不增加肝肾毒性。     

肝移植患者应用无激素与早期激素撤停免疫抑制方案的评价

背景:国内外均出现了肾移植后联合应用单克隆抗体的早期激素撤停或半量激素应用方案,研究发现减少激素应用并未明显增加排斥反应的发生,但能否将单克隆抗体完全替代激素的方案安全有效地应用于肝移植患者,目前较少见报道.目的:对肝移植患者应用无激素和早期激素撤停两种免疫抑制方案的观察,评价两种方案的临床疗效及安全性.方法:肝癌肝移植患者80例,其中33例患者应用巴利昔单抗诱导的无激素免疫抑制方案(他克莫司+酶酚酸酯+巴利昔单抗)作为实验组;另47例患者应用早期激素撤停方案(他克莫司+酶酚酸酯+激素)作为对照组.对照组激素于移植后第1天以后逐日减量,至移植后1个月停用.随访观察两组患者排斥率、感染率、1年内肿瘤复发率及1年生存率.结果与结论:实验组患者感染率、1年内肿瘤复发率明显低于对照组(P<0.05);两组患者排斥反应发生率及1年生存率差异无显著性意义(P>0.05).结果提示肝癌肝移植患者可以安全有效的应用无激素的巴利昔单抗免疫抑制方案,移植后感染率、肿瘤复发率明显低于激素治疗方案,并且不增加急性排斥反应的发生率.     

胰肾联合移植早期治疗临床研究

目的探讨胰肾联合移植术后治疗措施。方法1例胰肾联合移植术后给以免疫抑制、小剂量肝素化和胰岛素替代治疗,监测移植胰、肾功能及并发症情况。结果胰腺功能恢复顺利,1个月后脱离胰岛素,血糖维持正常;移植肾功能1周恢复正常,随后出现排斥反应,相应治疗后改善;术后3周出现下消化道出血。结论胰肾联合移植是针对IDDM合并终末期肾病的有效治疗措施。早期胰岛素替代治疗有利于移植胰功能的逐渐恢复。早期小剂量肝素化,有利于减少移植胰血栓形成的几率。     

胰肾同期移植术式选择与并发症分析

【目的】总结胰液膀胱引流(BD)与肠道引流(ED)两种胰肾一期移植(SPK)手术方式,分析术后并发症发生情况、原因和处理方式。【方法】12例Ⅰ型糖尿病(IDDM)合并尿毒症患者施行了SPK,最初2例为BD术式,另10例为改进的ED术式。术后早期采用他克莫司(FK506)／环孢素A(CsA) 霉酚酸酯(MMF) 皮质激素 抗淋巴细胞球蛋白(ALG)或抗CD25单抗四联诱导治疗．以后改为三联维持。抗凝治疗使用肝素、低分子右旋糖酐。【结果】12倒手术均获得成功,术后移植胰、移植肾功能恢复良好,停用外源性胰岛素。4例出现移植肾急性排斥,其中3例治疗后逆转,1例移植肾功能丧失。手术并发症包括：腹腔感染3例,切口感染2例。分别经引流换药治疗后二期愈合;肾周血肿2例．经手术探查清理后好转。多与抗凝剂短期应用过量有关。远期并发症：2例BD术式患者长期存在化学性膀胱炎．其中1例发生2次反流性移植物胰腺炎．经保守治疗好转。所有病例术后均未发生吻合口漏和移植物血管栓塞等严重并发症。【结论】改进的ED—SPK术式安全、简单,远期并发症少,是治疗IDDM合并尿毒症的理想方法;但应积极预防术后早期出血、感染并发症。     

彩色多普勒血流成像在胰肾联合移植术后的应用价值

目的探讨彩色多普勒血流成像(CDFI)在胰肾联合移植(SPK)术后的应用价值.方法用CDFI定期连续观测10例胰肾联合移植术后患者的声像图特征和动静脉血流变化.结果10例胰肾联合移植术后患者早期均出现移植胰腺体积增大,形态饱满,内部回声减低,胰头及胰尾部增大较胰体部明显,差异存在显著性意义(P＜0.05),多在十数天至1个月后恢复正常;其中2例术后移植肾体积增大,实质增厚,各级动脉血流阻力指数(RI)增高(均在0.71～1.0之间),移植胰腺周围出现局限性积液暗区,供体腹腔干动脉RI波动在0.67～0.78之间,CDFI提示急性排斥反应;1例移植胰腺体积明显增大,内部实质回声不均,胰周积液不断增多,供体腹腔干内动脉RI＜0.70,移植肾声像图正常,CDFI诊断移植胰胰腺炎;另外,CDFI诊断右侧髂外静脉及属支部分栓塞1例;提示移植胰腺供体腹腔干动脉血栓栓塞1例.结论CDFI在胰肾联合移植中具有重要的应用价值.     

Sensitivity of whole-blood T lymphocytes in individual patients to tacrolimus (FK 506): impact of interleukin-2 mRNA expression as surrogate measure of immunosuppressive effect

BACKGROUND: To optimize immunosuppressive treatment in individual transplant patients, functional measurements of the effects of tacrolimus (FK 506) are of clinical importance. Previous investigations have demonstrated the occurrence of tacrolimus-resistant production of interleukin-2 (IL-2) in vitro, which may explain in part why rejection episodes are still a frequent problem despite attainment of therapeutic blood concentrations and HLA matching. However, an adequate surrogate marker to define the tacrolimus response in individual patients has not been established. METHODS: We investigated the immunosuppressive effects of tacrolimus on anti-CD3/anti-CD28 T-cell costimulation in a human whole-blood assay, analyzing T-cell proliferation, activation marker expression (CD25, CD69), IL-2 protein expression, and cytokine mRNA expression in vitro (n = 11 healthy individuals). We also quantified IL-2 mRNA expression in patients undergoing tacrolimus (n = 4) or cyclosporin A (CsA; n = 4) monotherapy before ex vivo living-donor kidney transplantation. RESULTS: T-cell proliferation; CD25, CD69, and IL-2 concentrations; and IL-4 mRNA were significantly decreased in vitro. In contrast, cytokine mRNA profiles revealed variable tacrolimus sensitivity. Whole-blood samples from 3 of 11 healthy individuals demonstrated marked suppression of IL-2 mRNA expression (>50%) when tacrolimus was administered in vitro. When CsA was added to whole-blood cultures, the influence on IL-2 mRNA expression was comparable to that of tacrolimus in 9 of 11 individuals. Two individuals responded conversely, indicating that differences in the in vitro response to tacrolimus and CsA among individuals may be attributable to potential heterogeneity in the involvement of the CD28 pathway. Kinetic profiles of IL-2 mRNA expression also revealed individually distinct degrees of calcineurin inhibitor sensitivity in patients undergoing tacrolimus or CsA monotherapy before living-donor kidney transplantation. CONCLUSIONS: Our results suggest an individual degree of calcineurin inhibitor sensitivity of activated whole-blood lymphocytes based on IL-2 mRNA expression. Our approach is potentially valuable for identifying transplant patients in whom IL-2 mRNA expression is unaffected or even enhanced after initiation of immunosuppressive therapy. Such individuals may be less sensitive to the immunosuppressive agent and therefore at increased risk of transplant rejection. Prospective studies are necessary to determine the correlation of IL-2 mRNA expression with the clinical risk of transplant rejection.     

Impact of simultaneous pancreas and kidney transplantation on progression of coronary atherosclerosis in patients with end-stage renal failure due to type 1 diabetes

OBJECTIVE: Mortality in type 1 diabetic patients with end-stage renal failure is high and dominated by coronary atherosclerotic events. With regard to prognosis, simultaneous transplantation of pancreas and kidney (SPK) may be superior to kidney transplantation alone (KTA) in type 1 diabetic patients, because normalization of blood glucose levels may reduce progression of coronary atherosclerosis and because it is well known that progression of coronary atherosclerosis is one of the major factors that determines clinical prognosis. However, no data are available on progression of coronary atherosclerosis after SPK. RESEARCH DESIGN AND METHODS: We performed an observational angiographic study comparing progression of coronary atherosclerosis, analyzed with quantitative coronary angiography, in patients with (n = 26) and those without (n = 6) a functioning pancreas graft after SPK, to test the hypothesis that normalization of blood glucose levels by SPK may indeed reduce progression of coronary atherosclerosis in type 1 diabetic patients and thereby improve prognosis. RESULTS: Mean follow-up was 3.9 years. Average glucose control was significantly worse for the patients without a pancreas graft than for patients with a functioning pancreas graft: 11.3 (SD 3.5) vs. 5.9 mmol/l (SD 1.1) (P = 0.03). Mean segment diameter loss (progression of diffuse coronary atherosclerosis) was 0.024 mm/year (SD 0.067) in patients with a functioning pancreas graft, compared with 0.044 mm/year (SD 0.038) in patients in whom the pancreas graft was lost. Minimum obstruction diameter loss (progression of focal coronary atherosclerosis) was 0.037 mm/year (SD 0.086) in patients with a functioning pancreas graft compared with 0.061 mm/year (SD 0.038) in patients in whom the pancreas graft was lost. Regression of atherosclerosis occurred in 38% of patients with a functioning pancreas graft compared with 0% of patients of whom the pancreas graft was lost (P = 0.035). CONCLUSIONS: Our study provides, for the first time, evidence that in patients who have undergone SPK, progression of coronary atherosclerosis in patients with a functioning pancreas graft is reduced compared with patients with pancreas graft failure. Our observation is an important part of the explanation for the observed improved mortality rates reported in type 1 diabetic patients with end-stage renal failure after SPK compared with KTA. In light of these findings described above, SPK must to be carefully considered for all diabetic transplant candidates.     

门静脉回流与体静脉回流对胰肾联合移植效果影响的系统评价

目的系统评价胰肾联合移植（simultaneous pancreas-kidney transplantation，SPK）内分泌门静脉回流和体静脉回流两种术式术后移植物存活率、受者存活率和并发症发生率有无区别。方法计算机检索EMbase（1974～2008．1）、PubMed（1970～2008．1）、Cochrane图书馆（2008年第l期）和中国生物医学文献数据库（1978～2008．1），纳入3篇胰肾联合移植内分泌引流两种术式比较的随机对照试验。采用Cochrane协作网的系统评价方法评价纳入研究质量，并提取有效数据进行统计分析。结果最终纳入3个RCT共401例胰肾联合移植进行评价。Meta分析结果显示：胰腺移植内分泌引流的两种术式之间，仅1个研究（共82例）报道门静脉回流术式的3年和5年移植胰腺存活率优于体静脉回流术式（P=0．03，P=0．05），但所有研究的移植胰腺、移植肾脏及受者的各时间点存活率和各种并发症如排斥反应、移植物血栓形成和感染等发生率差异无统计学意义。结论现有研究结果显示，胰肾联合移植内分泌引流两种术式术后移植物存活率、受者存活率和并发症发生率相同。但由于现有临床研究样本量少，上述结论尚需大样本、长期随访的高质量随机对照研究证实。     

胰肾一期联合移植术后影像学检查

目的 探讨胰肾一期联合移植(SPK)术后影像学检查的临床价值。方法 于1998年12月至2000年1月期间的5例SPK术后的影像学检查中，5例均行胸片及彩色多普勒血流图(CDFI)检查，其中2例行数字减影血管造影检查。结果 在SPK术后影像学检查的阳性结果中，胸片诊断为肺部感染者2例，CDFI诊断急性排异反应2例，DSA诊断移植胰腺的供血动脉内血栓者1例。4例患者已健康存活了2年左右，其中1例因移植胰腺血管内血栓形成，于术后33天切除移植胰腺。1例因排斥反应于术后第47天死于急性心功能衰竭。结论 胸片与CDFI检查是SPK术后并发症的非侵袭性的首选诊断方法，DSA检查是SPK术后血管并发症合理而可靠的诊疗手段。     

Choice of antibody immunotherapy influences cytomegalovirus viremia in simultaneous pancreas-kidney transplant recipients

OBJECTIVE: Simultaneous pancreas-kidney (SPK) transplantation in type 1 diabetic patients requires immunotherapy against allo- and autoreactive T-cells. Cytomegalovirus (CMV) infection is a major cause for morbidity after transplantation and is possibly related to recurrent autoimmunity. In this study, we assessed the pattern of CMV viremia in SPK transplant recipients receiving either antithymocyte globulin (ATG) or anti-CD25 (daclizumab) immunosuppressive induction therapy. RESEARCH DESIGN AND METHODS: We evaluated 36 SPK transplant recipients from a randomized cohort that received either ATG or daclizumab as induction therapy. Patients at risk for CMV infection received oral prophylactic ganciclovir therapy. The CMV DNA level in plasma was measured for at least 180 days using a quantitative real-time PCR. Recipient peripheral blood mononuclear cells were cross-sectionally HLA tetramer-stained for CMV-specific CD8(+) T-cells. RESULTS: Positive CMV serostatus in donors was correlated with a higher incidence of CMV viremia than negative serostatus. In patients at risk, daclizumab induction therapy significantly prolonged CMV-free survival. CMV viremia occurred earlier and was more severe in patients with rejection episodes than in patients without rejection episodes. CMV-specific CD8(+) T-cell counts were significantly lower in patients developing CMV viremia than in those who did not. CONCLUSIONS: Despite their comparable immunosuppressive potential, daclizumab is safer than ATG regarding CMV infection risk in SPK transplantation. ATG-treated rejection episodes are associated with earlier and more severe infection. Furthermore, high CMV-specific tetramer counts reflect antiviral immunity rather than concurrent viremia because they imply low viremic activity. These findings may prove valuable in the discussion on both safety of induction therapy and recurrent autoimmunity in SPK and islet transplantation.     

Pancreas transplantation at Mayo: III. Multidisciplinary management

Although pancreas transplantation is a complicated procedure, a good level of success has been achieved because of the introduction of cyclosporine for immunosuppression, improved methods for diagnosing rejection, and a multidisciplinary approach to management. Our immunosuppressive regimen was quadruple therapy with induction by using Minnesota antilymphoblastic globulin. A biopsy technique was instituted in which the pancreas specimens were obtained under cystoscopic direction during episodes of hypoamylasuria. The criteria for rejection episodes were not only biochemical abnormalities but also histologic confirmation and a follow-up to exclude other causes of graft dysfunction. Infectious disease management included use of oral selective bowel decontamination for 3 weeks after transplantation. At the Mayo Clinic between October 1987 and December 1988, 16 patients received pancreaticoduodenal allografts (both kidney and pancreas in 13 and pancreas only in 3 after a prior successful kidney transplantation). In two pancreas and one kidney allograft, function was lost. One patient died of multiorgan failure. The cystoscopically directed biopsy technique was performed 23 times with minimal complications and a 93% success rate. The metabolic results have been excellent; the glycosylated hemoglobulin level was normal 3 to 6 months after transplantation. The quality of life was significantly improved in almost all patients. Nutritional assessment revealed little deterioration after transplantation. With a multidisciplinary approach, the needed answers about the effect of pancreas transplantation on the degenerative complications of diabetes should be forthcoming.