改良胰液空肠引流式胰肾同期联合移植35例报告

目的报告应用改良胰液空肠引流式胰、十二指肠及肾同期联合移植(SPK)的外科技术治疗35例胰岛素依赖型糖尿病并发尿毒症的近期效果。方法2000年6月-2006年1月,35例胰岛素依赖的糖尿病合并尿毒症患者接受SPK,移植胰的外分泌采用空肠内引流,不作Roux-en-Y型吻合。移植肾平均冷缺血时间为(6．92±2．17)h,移植胰平均冷缺血时间为(9．65±2．02)h。术后早期采用他克莫司、霉酚酸酯及皮质激素预防排斥反应,同时以抗淋巴细胞球蛋白或抗CD25单克隆抗体诱导治疗。结果围手术期患者存活率达97．1％(34／35),存活病例全部停用胰岛素,平均停用胰岛素时间为(8．3±4．5)d,空腹血糖恢复正常时间为(13．4±8．9)d。术后3周口服糖耐量试验、胰岛素和C肽释放试验显示移植胰功能完全正常。血淀粉酶恢复正常时间平均为(9．3±7．0)d。肾功能延迟恢复(DGF)5例,血肌酐恢复正常时间平均为(58．2±16．8)d,其余30例血肌酐恢复正常时间平均为(7．7±5．4)d。术后主要外科并发症为移植胰伤口感染、胰十二指肠-空肠出血和移植肾周围出血。3例(8．6％)因并发症再次手术,未发生与胰液引流术式相关的并发症如胰漏、肠漏、腹腔脓肿及肠梗阻等。结论SPK是治疗1型和部分2型糖尿病并发尿毒症的有效方法;改进的胰液空肠引流术式(不作Roux-en-Y吻合)有助于降低胰液空肠引流术式的术后早期并发症发生率。     

胰、肾同期联合移植治疗糖尿病合并尿毒症40例

目的 报告40例胰、肾同期移植(SPK)治疗糖尿病合并尿毒症的结果 及经验.方法 共40例糖尿病合并尿毒症病人接受SPK,平均年龄为(45.8±8.2)岁.供肾先植入左侧髂窝.供胰植入右下腹腔,移植胰动脉与右侧髂外动脉端侧吻合,移植胰静脉与右侧髂外静脉端侧吻合.其中胰液膀胱引流术式2例,改进的胰液空肠引流术式38例.移植肾平均冷血时间为(7.13士2.02)h,移植胰平均冷缺血时间为(9.95±2.01)h.术后早期采用皮质激素+霉酚酸酯+他克莫司(36例)/环孢素A(2例)+抗淋巴细胞球蛋白(ALG)或抗CD25抗体四联诱导治疗,以后改为三联维持.结果 受者、移植肾和移植胰6个月存活率均为97.5%,1年存活率均为94.8%,受者、移植胰和移植肾3年存活率分别为94.8%、84.3%和84.3%.39例停用胰岛素,平均停用胰岛素时间为(6.87士6.80)d,空腹血糖平均恢复正常时间为(13.68士9.05)d.术后3周口服糖糖耐量试验、胰岛素和C肽释放试验显示移植胰功能完全正常.血淀粉酶恢复正常时间平均为(10.24±7.72)d.肾功能延迟恢复(IX;F)8例,血肌酐恢复正常时间平均为(52.75±20.01)d,其余30例血肌酐恢复正常时间平均为(8.03±7.39)d.术后主要外科并发症为移植胰伤口感染、胰十二指肠一空肠出血和移植肾周出血,3例(7.9%)因并发症再次手术,未发生与胰液引流术式相关的并发症如胰漏、肠漏、腹腔脓肿及肠梗阻等.结论 (1)SPK是治疗糖尿病合并尿毒症的有效方法 ;(2)改进的胰液空肠引流术式更简化、安全,更符合生理.     

两种胰液引流术式的胰肾联合移植临床效果比较

目的 分析53例糖尿病并终末期肾病患者行同期胰肾联合移植不同胰液引流术式的临床效果对比。方法 2010年5月至2019年12月广西医科大学第二附属医院移植医学中心完成了53例同期胰肾联合移植手术,其中胰液膀胱引流（bladder drainage,BD）术式22例,胰液空肠引流（enteric drainage,ED）术式组31例。对比两组不同胰液引流术式受者的移植肾功能延迟恢复发生率、术后移植胰腺功能延迟恢复发生率、胰腺冷缺血时间、移植胰腺1年生存率、手术时间、再手术率、术中总输血量、术后1个月血糖变化、其他并发症等。结果 53例胰肾联合移植手术成功,随访4～90个月,在22例BD术式中,有1例患者发生坏死性胰腺炎,切除胰腺。3例患者出现移植肾功能延迟恢复,有1例患者移植肾功能延迟恢复,恢复有尿后发生出血性膀胱炎,后并发肺部感染而死亡。移植后（14.2±5.1）d空腹血糖降至正常,（9.5±4.2）d停止使用胰岛素,（10.4±6.5）d肾功能恢复正常。平均住院时间为（21.4±7.3）d,术后出现并发症有移植胰腺静脉血栓2例,泌尿系感染1例,移植胰淋巴漏1例,切口感染1例,他克莫司...     

胰液肠腔引流式胰十二指肠及肾一期联合移植一例报告

目的 总结胰液肠腔引流式胰肾联合移植的经验，探讨联合移植用药量，减少并发症。方法 对1例I型糖尿病并发尿毒症患者施行胰液肠腔引流式一期联合移植，术后早期应用他克莫司（FK506）、霉酚酸酯（MMF）、皮质激素和抗胸腺细胞球蛋白（ATG）进行免疫抑制治疗。监测胰腺、肾的功能恢复情况。结果 术后第3d，受者血肌酐、尿素氮恢复正常，术后第4d出现FK506中毒，致尿量减少，经调整FK506用量及进行血液透析过度无尿期，术后第10d，肾功能恢复正常；术后第5d停用胰岛素，移植胰内外分泌功能正常，术后第20d并发消化道出血，使用善得定及施他宁治疗痊愈。无其它外科并发症。结论 （1）胰液肠腔引流术式优于胰液膀胱引流术式；（2）胰液肠腔引流式胰、十二指肠及肾联合移植是治疗胰岛素依赖型糖尿病并发尿毒症的有效方法；93）优质的供者及良好的配型可减少并发症的发生。     

改良的胰液空肠引流式胰、肾一期联合移植(附2例报道)

目的 报告2例改良的胰液空肠引流式胰、十二指肠及肾联合移植的外科技术和治疗胰岛素依赖型糖尿病并发尿毒平的效果。方法 2000年6-9月,2例胰岛素依赖型糖尿病并发尿毒症的患者接受胰、十二指肠及肾一期联合移植,移植胰的外分泌采用空肠内引流,不作Roux-en-Y型吻合,结果 移植后,立即停用胰岛素,肾功能1-5d恢复正常,无外科并发症,未发生排斥反应,患者目前已分别存活5个月和2个月,移植胰和移植肾功能均正常,一般情况良好。结论 改良的胰液空肠引流式胰、十二指肠及肾联合移植技术简单、安全,是治疗I型糖尿病并发尿毒症的较好术式。     

改良胰液引流方法行胰肾联合移植1例

胰肾联合移植已经成为治疗I型糖尿病合并尿毒症的首选方法。胰液外分泌的处理一直是胰腺移植的难点所在，我院于2006年1月采用改良胰液空肠引流术式为1例患者成功施行胰肾联合移植。目前患者／移植物存活良好，现报告如下：     

在一个单位进行的100次胰腺移植

明尼苏达大学于1966年12月18日首先在一位患尿毒症的糖尿病病人同时进行了肾和胰腺移植。自1966年12月31日至1973年3月19日共施行了14例胰腺异体移植。1例为一段胰腺移植,胰管予以结扎;4例为胰十二指肠移植和十二指肠造口术以引流胰液;8例为胰十二指肠移植,十二指肠(供体)与空肠(受体)Y 型吻合;1例为全胰移植,供体 Vater壶腹吻合于受体空肠。除4例外,10例同时接受了异体肾移植,肾和胰腺均来自同一供体。胰腺功能维持的时间平均为3.0±3.5月,最长为12月,后者因     

改良式胰肾联合移植1例并文献复习

目的探讨改良式胰肾联合移植治疗2型糖尿病合并终末期肾病的移植效果。方法为1例2型糖尿病合并终末期肾病患者行改良式胰肾联合移植,其中移植胰腺的外分泌采用胰液空肠内引流术式,将供胰十二指肠节段与受体上段空肠直接行侧侧吻合。结果术后围手术期移植肾稳定泌尿,3800～4500ml/24h,3d后血清肌酐降至正常水平。术后胰腺功能恢复顺利,血、尿淀粉酶逐渐下降并稳定在正常范围,空腹血糖也于术后10d恢复至正常值范围以内。切口一期愈合,于术后两周出院。随访27个月移植肾功能正常,胰腺功能正常,未发生血栓、胰瘘、胰腺炎、排斥反应等并发症。结论改良式胰肾联合移植技术简单、安全,胰液经空肠引流更接近消化生理,是治疗糖尿病合并终末期肾病的有效手术方式。     

改良胰液空肠引流式胰肾一期联合移植一例

胰肾联合移植（SKPT）是治疗胰岛素依赖型糖尿病合并终末期尿毒症的理想方法。我院2004年7月6日成功地采用改良的胰液空肠引流术式行胰肾一期联合移植1例，取得了满意效果，报告如下。     

胰腺假性囊肿41例诊治体会

目的探讨胰腺假性囊肿的诊断及外科手术治疗方式。方法回顾性分析行手术治疗的41例胰腺假性囊肿患者的临床资料,其中行单纯囊肿外引流术7例（17．1％）,单纯囊肿切除10例（24．4％）,囊肿及胰尾部切除＋脾切除术3例（7．3％）,囊肿空肠Roux-en-Y吻合18例（43．9％）,囊肿胃吻合3例（7．3％）。结果术后发生并发症8例（19．5％）,1例囊肿胃吻合术患者术后2d出现消化道出血,经非手术治疗而痊愈出院;2例患者（单纯囊肿外引流术1例,囊肿空肠Roux-en-Y吻合1例）早期出现不全性肠梗阻,经过保守治疗出院;2例单纯囊肿外引流术患者术后出现胰瘘,1例胰瘘经保守治疗治愈,另外1例因长期胰瘘而再行瘘管空肠吻合术而治愈;1例囊肿空肠Roux-en-Y吻合术后出现逆行感染,经抗炎保守治疗后病情缓解;全组切口感染2例,1例保守换药,另1例换药后行二期缝合均获痊愈。无手术死亡病例。随访37例,时间6个月～5年,平均（3．3±1．9）年,2例单纯囊肿切除术患者于术后1年复发,经保守治疗症状缓解。结论胰腺假性囊肿在经保守治疗渡过急性期后,应根据需要采取个体化的外科治疗方案。     

Metabolic effects of a corticosteroid-free immunosuppressive regimen in recipients of pancreatic transplant

BACKGROUND: A corticosteroid (CS)-free immunosuppressive regimen may be considered less diabetogenic than treatments including CSs principally after pancreas transplantation. METHODS: To test whether a CS-free immunosuppressive treatment is metabolically superior to a regimen including CSs, we prospectively studied 19 CS-free simultaneous pancreas and kidney (SPK) transplant recipients (body mass index=22+/-1 kg/m2; cyclosporine dose=400+/-19 mg/kg/day; azathioprine dose=77+/-8 mg/day; basal plasma C-peptide=1.3+/-0.12 ng/mL) and 12 matched CS-treated SPK transplant recipients (prednisone dose=9+/-1 mg/day; basal C-peptide=2.2+/-0.2 ng/mL) by means of the 6,6-2H(2)-glucose infusion and the euglycemic insulin clamp (1 mU/kg/min, insulin infusion rate). In addition, six renal transplant recipients receiving a CS-free regimen were also studied as a control group. RESULTS: In the postabsorptive state, CS-treated SPK transplant recipients demonstrated comparable plasma glucose levels but higher plasma insulin levels than CS-free SPK transplant recipients. Plasma triglyceride levels were significantly higher in CS-treated SPK patients than in CS-free SPK patients (1.16+/-0.16 mg/dL vs. 0.88+/-0.08; P<0.05). High-density lipoprotein and apoprotein A(1) levels were similar in both groups. No difference was observed in pyruvate, lactate, beta-OH-butyrate, and basal endogenous glucose production in all three groups of patients studied. During euglycemic hyperinsulinemia, the inhibition of endogenous glucose production and the stimulation of tissue glucose disposal were not statistically different among the three groups. CONCLUSIONS: SPK recipients receiving chronic low-dose CS maintenance therapy do not present a lower glucose disposal than CS-free recipients. Nonetheless, this is obtained at the expense of a higher endogenous insulin secretion, which can cause an alteration of the triglyceride profile.     

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.     

Enteric drainage of a pancreas allograft is safe for patients with celiac sprue

Enteric drainage of exocrine secretions in whole organ pancreas transplantation is generally avoided in patients with pre-existing small bowel disease; however, bladder drainage is associated with a 20% rate of urinary tract-related complications. This is a case report of a type 1 diabetic patient with celiac sprue and renal failure. We performed a simultaneous cadaveric kidney pancreas transplant enterically draining the exocrine pancreas. There were no complications. The patient is now more than 6 months post-transplant with excellent function of both renal and pancreas allografts. We conclude that enteric drainage of pancreas allografts in patients with celiac sprue may be performed safely. Whole organ pancreas transplantation is being performed with greater success than ever before, mostly as a result of lessons learned from past experience (1). Enteric drainage of allograft exocrine secretions is preferred for simultaneous pancreas/kidney (SPK) recipients to avoid urinary tract complications associated with bladder drainage. However, most agree that diabetics with pre-existing bowel disease should have bladder drainage of allograft exocrine secretions, so as to prevent the devastating complication of a bowel leak. We describe here a successful case of enteric drainage of an SPK transplant in a patient with celiac sprue. We believe that, when carefully performed, enteric drainage of pancreas allografts is a safe approach for diabetic patients with celiac sprue, and may avert the serious complications associated with bladder drainage.     

Improved solitary pancreas transplant graft survival in the modern immunosuppressive era

The results of solitary pancreas (SP) transplantation have traditionally lagged behind those of simultaneous pancreas-kidney (SPK) transplantation. This is one of the chief factors that has limited the wide-scale application of SP transplantation in nonuremic type I diabetic patients. The purpose of this study is to report our present experience with SP transplantation and compare it to a prior experience. Twenty-three SP transplants (14 PAK, 4 PTA, and 5 PASPK) performed since January 1997 were compared to 56 SP transplants (53 PAK, 1 PTA, and 2 PASPK) performed before 1994. Between 1993 and 1997, SP transplants were not performed because of high morbidity in the early experience. Early SP transplants were performed using bladder drainage of exocrine secretions, and enteric drainage without a Roux-en-Y was used in the recent series. In the early era, immunosuppressive therapy included cyclosporine (CsA), azathioprine (AZA), corticosteroids, and in half of the patients, ALG or OKT3. Recent SP transplants received tacrolimus (TAC). mycophenolate mofetil (MMF), corticosteroids, and induction with either anti-thymocyte globulin (n = 9), OKT3 (n = 1), daclizumab (n = 5), or basiliximab (n = 8). The 1-year Kaplan-Meier patient survival was 85% in the early era and 100% in the recent group of patients (p = 0.08). In the previous era, four patients suffered significant decrement in renal function, necessitating dialysis or kidney transplantation following pancreas transplantation. All patients transplanted since 1997 maintain near prepancreas transplant levels of renal function (mean pretransplant serum creatinine (Cr) 1.3 +/- 0.3 mg/dl vs, mean current Cr 1.4 +/- 0.4 mg/dl, p = NS]. The 1-year Kaplan-Meier graft survival (insulin independence) of recent SP transplants was 87%, whereas for prior SP transplants it was 19% (p = 0.0001). The rate of acute pancreas rejection was significantly different between the two groups. Of early SP transplants, 76% experienced at least one rejection episode within the first year. In contrast, 35% of recent SP transplants suffered acute rejection during the same time period (p = 0.04). Current experience with SP transplantation demonstrates improved graft survival and reduced rejection rates with the use of newer immunosuppressive agents.     

Renal hemodynamic effects of somatostatin are not related to inhibition of endogenous insulin release

BACKGROUND: Somatostatin inhibits endocrine and exocrine secretions and exerts renal vasoconstriction. The mechanism underlying somatostatin's vascular effects is unknown. Since insulin can cause vasodilation, we hypothesized that removal of basal insulin release by somatostatin may contribute to somatostatin-induced renal vasoconstriction. METHODS: The study was conducted in different protocols comprising forty-six healthy male volunteers. Randomized studies were performed to compare the effects of somatostatin alone (0.1 microg/kg/min) to the effects of somatostatin + low dose insulin (0.1 mU/kg/min), the effects of somatostatin + low dose insulin to the effects of somatostatin + high dose insulin (1.5 mU/kg/min), and the effects of insulin (1.5 mU/kg/min) + somatostatin. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured with the para-aminohippurate (PAH) and the inulin clearance technique, respectively. Blood pressure and pulse rate were measured non-invasively. RESULTS: Somatostatin alone decreased GFR (-14 +/- 6%, P < 0.001) and RPF (-16 +/- 7%, P < 0.001) whereas systemic hemodynamics were unchanged. Preceding or concomitant infusion of insulin at high doses (insulin plasma concentration of 127 +/- 25 or 144 +/- 17 microU/mL) but not co-infusion with low dose insulin (insulin plasma concentration of 11 +/- 3 microU/mL) mitigated or reversed the vasoconstrictive actions of somatostatin on GFR and RPF. CONCLUSIONS: Somatostatin induces marked renal vasoconstriction and exogenous restoration of fasting insulin concentrations does not influence the renal vascular effects. Therefore, it is unlikely that somatostatin-induced vasoconstriction is due to removal of basal insulin. Plasma insulin concentrations in the high postprandial range can reverse somatostatin-induced renal vasoconstriction, suggesting functional antagonism.     

Differential effects of preexisting uremia and a synchronous kidney graft on pancreas allograft functional survival in rats.

Pancreas transplant results have been better in uremic recipients of a simultaneous kidney than in nonuremic recipients of a pancreas alone. We studied the relative effect of uremia versus a double transplant on functional survival by performing bladder-drained pancreas transplants alone (PTA), kidney transplants alone (KTA), and simultaneous pancreas/kidney (SPK) transplants from Buffalo donors to diabetic Lewis rat recipients that were or were not made uremic 2-3 weeks before by 1 4/5 native nephrectomy. Pancreas graft exocrine function was monitored by urinary amylase (UA). In the PTA and SPK recipients made diabetic by streptozotocin, endocrine function was monitored by measuring nonfasting plasma glucose (PG) levels. Kidney graft function was monitored by plasma creatinine (Cr). Rejection of the endocrine pancreas was defined as an increase of PG to greater than 200 mg/dl; of the exocrine pancreas, as a decline in UA to less than 6000 U/L or to less than 100 U/24 hr; and of the kidney, as an elevation of Cr to greater than 3 mg/dl. The mean functional survival times (MST) of both the endocrine (12.0 +/- 2.1 versus 10.1 +/- 1.1 days, P = 0.036) and exocrine (8.0 +/- 2.1 versus 6.3 +/- 1.3 days, P = 0.016) components of the pancreas grafts were significantly longer in SPK than in PTA recipients. The MST of kidney allografts, however, was not significantly longer in nonuremic SPK than nonuremic KTA recipients (6.7 +/- 1.4 versus 5.7 +/- 0.7 days, P = 0.13). In parallel experiments in recipients immunosuppressed with cyclosporine, the graft survival times were longer, but the relative differences between the PTA, SPK, and KTA groups persisted. Histologically, lymphocyte infiltration began in the two organs almost simultaneously, but the severity of the rejection was more vigorous in the kidney than in the pancreas in doubly grafted rats, and destruction of pancreas grafts progressed more slowly in SPK than in PTA recipients. Preexisting uremia delayed pancreas rejection in both SPK (exocrine 10.6 +/- 2.3, P = 0.032, and endocrine 14.8 +/- 3.4 days, P = 0.065, versus nonuremics) and PTA (exocrine 8.5 +/- 1.7, P = 0.007, and endocrine 12.6 +/- 2.5, P = 0.026, versus nonuremics) nonimmunosuppressed recipients. The MST of kidney grafts was not significantly longer in uremic (8.9 +/- 2.8 days) than in nonuremic (6.7 +/- 1.4 days) SPK recipients (P = 0.081). A synchronous kidney transplant and uremia independently down-modulate the rejection response to a pancreas graft, and a simultaneous pancreas graft has no detrimental effect on the survival of a kidney graft.(ABSTRACT TRUNCATED AT 400 WORDS)     

Bladder vs enteric drainage in simultaneous pancreas-kidney transplantation.

BACKGROUND: As a valid therapeutic option for patients with type 1 diabetes mellitus (IDDM) and secondary diabetic nephropathy, simultaneous pancreas-kidney (SPK) transplantation remains more undeveloped than other solid organ transplantations due to restrictions of surgical techniques, especially modes of exocrine pancreatic secretion. Enteric drainage (ED) has recently been increasingly popular due to the long-term complications with bladder drainage (BD). Objectives. Compare results of SPK transplants with enteric vs bladder exocrine drainage since the beginning of our experience with this type of transplantation. METHODS: From March 1998 to October 2004, 53 SPK transplants were performed, consisting of 30 with bladder drainage (BD) and 23 with enteric drainage (ED). Induction therapy included antilymphocyte globulin (ALG) or anti-CD25 monoclonal antibody. Maintenance regimen consisted of tacrolimus (TAC)/cyclosporine (CsA), mycophenolate mofetil (MMF) and steroids. RESULTS: Mean age of recipients was 39+/-7 in both groups. No anastomosis leakage occurred in either group. Surgical complications were not significantly different between the two groups. Incidence of acute rejection, major infections and cytomegalovirus disease were also similar. However, the BD group was characterized by a slight increase in number of urologic complications, metabolic acidosis and dehydration. The length of initial hospital stay was likewise comparable. All patients with a functional graft no longer required exogenous insulin. BD actuarial patient survival and graft three-year survival were 96 and 86%, respectively. For ED, the respective results were 97 and 91%, respectively. CONCLUSION: Compared with BD, perioperative morbidity is not increased by ED, and ED is not associated with increased long-term pancreas graft failure. These data suggest that ED is superior to BD and should be considered as the preferred technique for simultaneous pancreas-kidney transplants.     

Conversion of exocrine secretions from bladder to enteric drainage in recipients of whole pancreaticoduodenal transplants.

Between September 1984 and August 1991, 265 whole pancreaticoduodenal transplants were done at our institution, with bladder drainage of exocrine secretions through a duodenocystostomy. Seventeen patients subsequently underwent conversion from bladder to enteric drainage at 2 to 64 months after transplant. Eight conversion procedures were done to correct chronic intractable metabolic acidosis due to bicarbonate loss from the allograft: seven to alleviate severe dysuria, presumed secondary to the action of graft enzymes on uroepithelium; one to prevent recurrent allograft pancreatitis, presumed secondary to back pressure from the bladder; and one because of graft duodenectomy for severe cytomegalovirus duodenitis with perforation. None were done to correct technical complications from the initial transplant operation. The conversions were done by dividing the graft duodenocystostomy, then re-establishing drainage through a graft duodenal-recipient jejunal anastomosis. A simple loop of recipient jejunum was used for the duodenojejunostomy in 15 cases, and a Roux limb in two. One of those two cases had a previously created Roux limb that was available for use. The other was in the patient who underwent graft duodenectomy and subsequent mucosa-to-mucosa anastomosis of the pancreatic duct to a newly created Roux limb of jejunum. All patients experienced relief of their symptoms after operation. Two patients had surgical complications (12%), an enterotomy in one case, which was closed operatively, and an enterocutaneous fistula in the other case, which healed spontaneously with bowel rest and parenteral nutrition. The drawback to conversion is loss of urine amylase as a marker for rejection, particularly in recipients of solitary pancreas grafts (n = 5). In recipients of simultaneous pancreas-kidney (SPK) allografts (n = 12), the kidney can still be used to monitor for rejection (two with follow-up < 1 year, 10 with follow-up > 1 year). None of our solitary pancreas recipients, however, have lost graft function (follow-up, 10 to 36 months). The only pancreas allograft loss was in an SPK recipient who also rejected the kidney 6 months after conversion. She received a second SPK transplant with enteric drainage, and is insulin independent and normoglycemic 10 months after retransplantation. Patients converted for metabolic acidosis tended to have impaired renal function (mean creatinine, 2.14 +/- 0.98 mg/dL at time of conversion) due to chronic rejection, progression of native kidney diabetic nephropathy, or cyclosporine toxicity, and possibly could not compensate for bicarbonate loss from the pancreas allograft.(ABSTRACT TRUNCATED AT 400 WORDS)