移植肾自发性破裂的处理与随访

本文报道在302例324次同种肾移植术后发生移植肾自发性破裂19例22次。破裂时间为术后3周内,11例发生在CsA减量的交替期。15例破裂前出现典型的急性排斥反应。裂口1～4处不等。5例行移植肾切除;14例行保肾手术,术后3周内尿量及肾功能恢复正常。随访1～5年,保肾患者的人/肾长期存活率与同期移植肾未破裂者比较无显著性差异。     

移植肾破裂的治疗及预后

目的探讨移植肾破裂的治疗及预后。方法回顾性分析19例,21例次移植肾破裂患者临床资料。临床表现均为移植肾区突发疼痛,伴移植肾区肿胀、血压降低、少尿及血红蛋白降低。B超发现移植肾被膜不连续,移植肾周积液量明显增加。结果移植肾破裂时间平均为术后20 d。移植肾单一裂口15例,多发裂口4例。急诊手术治疗14例,其中移植肾切除5例,1例切除后死亡。移植肾破裂修补9例,其中3例修补后因再次破裂行移植肾切除,肾功能恢复5例,1例修补后死亡。保守治疗5例,其中2例因病情恶化行移植肾切除,肾功能恢复2例,死亡1例。病理证实移植肾破裂的主要原因为急性排斥反应和急性肾小管坏死。结论移植肾破裂主要原因为急性排斥反应和急性肾小管坏死,治疗应慎重采用保守治疗和修补术式,可采用移植肾切除术。     

自发性肾脏破裂出血18例

目的 提高对自发性肾脏破裂出血的诊治水平。方法 回顾分析18例自发性肾脏破裂出血患的临床资料。结果 肾包膜下出血10例，肾周血肿8例。其中错构瘤10例，保守治疗3例，肾切除2例，肿瘤剜除术5例；囊肿3例，保守治疗2例，探查血肿清除1例；移植肾破裂2例，均行移植肾切除；肾癌1例，行根治性肾切除；无明显原因2例，1例保守治疗，1例行血肿清除。结论 自发性肾脏破裂出血的治疗取决于原发病的性质及出血的严重程度。     

移植肾自发性破裂的保肾手术和长期疗效观察

移植肾自发性破裂占全部受肾者的0.3—8.5％,它是肾移植后的一种急性严重并发症,死亡率达9％。鉴于对其治疗意见不一,作者根据自己经验,对其治疗和长期疗效分析报告如下。临床资料夫利德利赫斯哈芬市立泌尿科医院肾移植中心,自1968.3—1980.3月共施行尸体肾同种移植434例,均按公认的标准手术方法进行,未做肾包膜剥离术,热缺血时间为0—50分,平均12分,冷缺血时间5—24小时,平均12小时。本组25例受肾者,在移植术后14天内,发生移植肾自发性破裂26次,以术后第6天出现最多,有一病例在4天内出现破裂2次。21例病人接受过透析治疗,12例病人在破裂时有高血压,血压在160/110毫米汞柱以上,7例病人在此期间正发生严重急性排     

移植肾动脉狭窄病因及介入治疗疗效分析

目的探讨移植肾动脉狭窄(TRAS)的病因、介入治疗的疗效及安全性。方法对2000年至2005年经移植肾动脉造影确诊为TRAS的23例患者的临床资料进行回顾性分析。男19例,女4例。年龄23～62岁,平均44岁。23例术后均采用环孢素(CsA)或他克莫司(FK506)加吗替麦考酚酯(MMF)加泼尼松(Pred)三联免疫抑制治疗,其中以CsA治疗为主者14例(60.9%),以FK506治疗为主者9例(39.1%)。结果23例TRAS患者中发生急性排斥反应(AR)者13例(56.5%);移植肾功能延迟恢复(DGF)者4例(17.4%);吻合技术原因致吻合口狭窄者1例(4.3%),移植术后1周切除移植肾,再次移植成功;TRAS原因不明者5例(21.7%)。经造影确诊为移植肾动脉狭窄时间为移植术后1周～4年,平均(12±11)个月。单纯吻合口狭窄12例,单纯主干狭窄9例,吻合口并主干狭窄1例,吻合口并受体髂动脉狭窄1例。22例经介入治疗,13例(59.1%)肾功能于1周内恢复,8例(36.4%)2～3周内恢复,1例(4.5%)随访3个月肾功能无变化;造影剂肾毒性导致血肌酐一过性升高者5例,发生移植肾动脉血栓和腹股沟血肿各1例。结论同种异体肾移植术后TRAS与移植肾血管吻合技术、AR及DGF有关。移植肾动脉造影是确诊金标准,一经确诊应立即行球囊扩张或血管内支架治疗,注意并发症的发生。     

肾移植术后早期无尿或少尿的诊治(附66例报告)

目的:探讨肾移植术后早期无尿或少尿的原因及诊治方法.方法:回顾性分析66例肾移植术后早期无尿或少尿患者的发生情况.并分别应用以FK506或CsA为主的免疫抑制剂(FK506/CA+MMF+Pred)等综合治疗方案.结果:66例肾移植术后早期无尿或少尿的主要原因是急性肾小管坏死(77.27%),其次是急性排斥反应(10.61%),其中有2例移植肾原发无功能和移植肾破裂、肾动脉栓塞各1例术后切除移植肾.FK506组的34例移植肾功能在术后5～35天内均恢复正常,CsA组有1例因急性排斥反应合并严重肺部感染而死亡,24例移植肾功能在术后7～48天内均恢复正常,3例血肌酐在142～215 μmol/L之间.结论:肾移植术后早期出现无尿或少尿后应及时分析原因,并给予相应的综合治疗.FK506+MMF+Pred的三联免疫治疗有助于移植肾功能的早期恢复.     

肾移植术后早期抗体介导的急性排斥反应三例

目的 探讨肾移植术后早期抗体介导的排斥反应(AMR)诊断和治疗.方法 2011年1月至2012年8月间确诊的肾移植术后早期急性AMR病例3例.移植前受者均有HLA致敏史,其中2例群体反应性抗体(PRA)曾为阳性,但移植前已转为阴性,另1例移植前PRA-Ⅱ类抗体为强阳性.3例术前补体依赖的细胞毒性实验均为阴性.移植后1周内均出现了抗HLA抗体水平的迅速升高伴急性移植肾功能衰竭.急性AMR确诊后采用反复多次血浆置换及静脉注射丙种球蛋白(或联用硼替佐米)治疗.结果 3例移植肾穿刺病理结果均符合急性AMR的诊断标准.1例因确诊时移植肾已破裂出血而切除移植肾;1例经4次血浆置换及丙种球蛋白治疗后抗体水平显著下降且病理损伤明显好转,于术后50 d移植肾功能完全恢复正常;1例经5次血浆置换及丙种球蛋白联合硼替佐米治疗后无明显好转,于术后24 d切除移植肾.结论 HLA预致敏患者即使PRA移植前已转阴都属于肾移植术后早期急性AMR的危险人群,当出现移植肾早期原发性无功能或移植肾功能急剧下降时,及时检测HLA抗体水平和移植肾穿刺活检对确诊急性AMR十分重要.血浆置换及丙种球蛋白(或联合硼替佐米)治疗是目前首选的方法,预后与干预早晚及病理损伤程度密切相关.     

他克莫司联合霉酚酸酯应用于胰肾联合移植的初步经验

目的 总结他克莫司(FK506)联合霉酚酸酯(MMF)应用于胰液膀胱引流式胰肾联合移植受者的初步经验. 方法 胰肾联合移植患者14例,术后应用FK506 0.07～0.15mg·kg-1·d-1加MMF 1.0～1.5 g/d加泼尼松25 mg/d三联免疫抑制治疗方案.采用微粒子酶免疫分析法每周测定口服FK506后全血峰谷浓度,依此调整剂量维持最初3个月内FK506全血浓度峰值10～20 μg/L,谷值5～15μg/L.并观察排斥反应的发生及药物的肝肾毒性. 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,血糖及肌酐水平恢复正常.随访18～70个月,平均34个月.存活1～3年者3例,3年～者1例,4年～者1例,>5年者4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2年肾功能良好.4例死亡,死因分别为术后急性右心功能衰竭、呼吸骤停、急性排斥反应及十二指肠瘘.胰肾联合移植术后各时期FK506全血峰、谷浓度差异均有统计学意义(P<0.05).术后共发生肾脏急性排斥反应4例次,肾毒性2例次,肝毒性1例次. 结论 FK506与MMF在药效上有协同作用,联合应用于胰肾联合移植具有良好的免疫抑制效果,能有效降低排斥反应发生率和提高移植物长期存活率.     

移植肾自发性破裂的诊治

目的：探讨移植肾自发性破裂的原因及防治措施。方法：回顾分析本院３９２例同种肾移植术后发生移植肾自发性破裂２０例临床资料。结果：发生率为５．１％。１４例保留肾脏功能，其中２例经保守治疗痊愈。６例肾切除者中有４例为急性排斥反应引起。结论：肾破裂的发生与排斥反应、肾缺血性损害、肾静脉引流不畅及尿路梗阻有关。对于出血量少、肾功能好者，可采用保守治疗。预防要从肾脏摘取与灌洗、植肾手术、合理应用免疫抑制剂、及     

B超引导下移植肾穿刺活检的临床应用价值

目的 探讨B超引导下移植肾穿刺活检的安全性及在移植肾功能损害病因诊断中的价值.方法 2003-2006年经皮移植肾穿刺活检52例.男37例,女15例.平均年龄35岁.术前均行彩超检查,超声定位下用Magnum保险式自动活检穿刺枪穿刺.活检组织行苏木素-伊红染色、PAS染色、Masson染色、六胺银染色,免疫荧光检查4μm冰冻切片,直接法行IgA、lgG、IgM和补体染色.依据Banff 97标准诊断.结果 病理检查结果为慢性/硬化性移植肾肾病(CAN)20例、急性/活动性排斥反应(AR)15例、急性肾小管坏死(ATN)4例、环孢素(CsA)肾毒性反应(CsA-NT)8例、移植肾肾炎(TGN)4例、高血压肾病(HN)1例.AR、ATN、CsA-NT和高血压肾病共28例,其中15例AR患者均予甲泼尼龙冲击3 d,10例将CsA或吗替麦考酚酯加量,5例将CsA转换为他克莫司,1例因放弃治疗而失肾,余14例获逆转.4例ATN经血液透析治疗1～4周后移植肾功恢复正常.5例急性CsA-NT者CsA减量后肾功能恢复,3例慢性CsA-NT者CsA更换为小剂量他克莫司后血肌酐稳定.经针对性治疗后,移植肾功能逆转23例(82%)、稳定4例(14%)、恶化1例(4%).1例高血压肾病者经降压护肾治疗,移植肾功能稳定.CAN、TGN 24例,经反复调整治疗方案后移植肾功能逆转13例(54%)、稳定5例(21%)、恶化6例(25%).结论 超声定位下Magnum自动活检枪行移植肾穿刺安全可靠,活组织病理检查对于肾移植术后肾损害的病因诊断、指导抗排斥反应治疗具有重要价值.     

Surgical repair of spontaneous renal allograft rupture: a new procedure

Background: The purpose of the present paper is to introduce a new surgical procedure using the external oblique aponeurosis (EOA) for repair of spontaneous renal allograft rupture. Methods: Thirty‐eight cases with spontaneous renal allograft rupture were encountered in 1000 consecutive kidney transplants between April 1991 and August 2000. Thirty‐three cases underwent surgical exploration with two grafts undergoing nephrectomy, while a further 31 were repaired using the new surgical procedure. The external oblique aponeurosis (EOA) from the incision was trimmed into 1 cm × 1 cm square pieces. A 2/0 Dexon suture was placed through each piece of the EOA, then through the parenchyma of the kidney perpendicular to the rupture. Each suture was then placed through another piece of EOA and tied. Results: Two repaired grafts were removed on day 7 and day 10, one due to graft re‐rupture and another with ischaemia secondary to irreversible acute rejection. The graft function of 29 cases had recovered completely at 30 days following surgical repair with one graft improving rapidly. Thirteen grafts were diagnosed as undergoing mild to moderate acute rejection, whereas a further 20 cases were considered to have acute tubular necrosis on histopathology. The allograft survival rate at 1 year and 5 years post grafting was 86% and 64%, respectively. No patients died from postoperative complications following repair using this procedure. Conclusions: Spontaneous renal allograft rupture is a relatively common post‐transplant complication secondary to either acute tubular necrosis or acute rejection. This new surgical procedure is proposed as a reliable and practical method of repair following graft rupture. Preservation of graft function and viability following rupture appears achievable both in the medium and long‐term.     

Spontaneous kidney allograft rupture

Spontaneous renal allograft rupture is one of the most dangerous complications of kidney transplantation, which can result in graft loss. This condition needs immediate surgical intervention. Conservative management has dismal results. Its prevalence varies from 0.3% to 3%. Rupture occurs in first few weeks after transplantation. Predisposing factors for graft rupture are acute rejection, acute tubular necrosis, and renal vein thrombosis. There are growing reports about successful results of repairing these ruptured kidneys. In this study, we reviewed the medical records of 1682 patients who received kidney allografts from living donors from 1986 through 2003. There were six (0.35%) cases of renal allograft rupture. All were preceded by acute graft rejection. They were treated with antirejection medications. In first three cases, the kidney allografts were removed because the procedure of choice in this situation is graft nephrectomy; but in three next cases we repaired the ruptured grafts with good results in two of them. In conclusion, the procedure of choice for kidney allograft rupture is graft repair.     

移植肾自发性破裂

目的　提高肾移植破裂救治成功率。方法　破裂肾修补止血,血肿清除,创口引流,加强抗排斥治疗、抗感染及全身支持疗法。结果　30例移植肾破裂,6例切除,24例保留手术取得成功,全部存活。结论　患者一般情况尚好,无中毒症状及较重合并症,移植肾色泽鲜艳、血供良好,均可保留肾手术。     

Renal allograft rupture caused by acute tubular necrosis

Renal allograft rupture is a rare but potentially lethal complication of kidney transplantation. A renal allograft recipient receiving quadruple immunosuppressive therapy developed a spontaneous allograft rupture 13 days after kidney transplantation. Warm ischaemia time during the transplant was 80 minutes. The ruptured kidney graft could not be salvaged because of the patient's haemodynamic instability. The histopathological examination showed interstitial oedema with severe acute tubular necrosis with no signs of acute rejection. The most common causes of renal graft rupture are acute rejection and vein thrombosis, while acute tubular necrosis may only rarely be responsible for this complication. Renal graft rupture may be the result of interstitial damage attributed both to the prolonged warm ischaemia time during the transplant and to post-transplant acute tubular necrosis in the absence of graft rejection. In those patients whose haemodynamic status cannot be stabilized by appropriate aggressive haemodynamic support therapy, graft nephrectomy should be considered the only definitive treatment.     

Surgical strategies in spontaneous rupture of renal allograft

The methods of surgical treatment of spontaneous rupture of renal allotransplant (RAT) were studied up in 21 patients. In 17 (80.9%) of patients the RAT rupture was caused by an acute reaction of rejection (ARR), in 14.3% of observations--by an acute necrosis of tubules, in 2 (9.5%)--by renal vein thrombosis and in 2 (9.5%)--by an ischemic damage of the transplant. Surgical treatment of the RAT spontaneous rupture (except the cases with rupture due to renal vein thrombosis) must be managed by the hemorrhage stoppage, the RAT tissues strain reduction (decapsulation and the cross-like capsulotomy), conduction of its intraoperative anticrisis and antiischemic defense with subsequent complex therapy for ARR and the transplant dysfunction. Application of such a tactics of treatment have permitted to secure the RAT and its functions in spontaneous rupture in 82.4% of observations. The transplant survival was registered in terms up to one year in 64.7% of observations.     

Conservative surgery of spontaneous rupture of renal grafts]

17 cases of spontaneous rupture of renal allografts were noted after 285 renal transplantations performed during the years 1967-1978. All ruptures occurred within the first two weeks after transplantation. Acute rejection, combined with hypertension, dialysis and/or anticoagulation seem to be the main etiological factors of graft rupture. Due to severe hemorrhage surgical exploration had to be performed in 15 patients. While removal of the graft was necessary in 4 patients the kidney could be preserved by tamponade and suture in 11 patients. 5 patients later lost their graft, due to chronic rejection, while 8 patients (6 of the 15 patients who needed surgical exploration) currently have satisfactory graft function.     

肝肾联合移植的临床经验

目的 探讨肝肾联合移植的适应证、手术技术、治疗经验及并发症防治。方法2001年10月至2005年3月进行肝肾联合移植13例。男12例，女1例。年龄41—66岁，平均54岁。原发病：多囊肝、多囊肾并尿毒症3例，酒精性肝硬化合并尿毒症2例，乙型肝炎肝硬化合并尿毒症7例，肾移植术后14年丙型肝炎肝硬化导致肝衰竭伴移植肾功能不全尿毒症1例。肝移植采用经典非转流原位肝移植术式和背驮式肝移植术式，肾移植为常规术式。病肝切除时注意细致分离第三肝门、创面及时止血。以抗胸腺细胞球蛋白或白细胞介素-2受体单克隆抗体作为免疫诱导，术后服用他克莫司、吗替麦考酚酯及激素维持免疫抑制治疗。患者门诊随访，复查血、尿常规．肝肾功能，他克莫司血药浓度以及移植物B超等。随访时间12—53个月。结果13例手术均成功。术后发生急性排斥反应1例，继发性出血1例，心肌梗死1例（死亡），胸腔积液4例，肺部感染3例（1例死亡）。除死亡病例外，所有并发症经相应治疗后逆转治愈。11例存活者肝肾功能正常，其中存活4年5个月者1例，存活3年以上者2例，2年以上者6例，1年以上者2例。1例49岁患者术后18个月死于心肌梗死，1例52岁患者术后13个月死于肺部巨细胞病毒感染。结论 肝肾联合移植是肝肾功能衰竭的有效治疗手段。娴熟的手术技巧和并发症的及时诊治是肝肾联合移植成功的关键。     

Surgical methods of correction of the renal transplantation complications

Surgical complications were studied, which occurred in 55 (20.37%) of 244 patients, to whom 270 renal allotransplantation (RAT) operations were performed. In 19 (34.6%) of recipients the urological complications were noted, in 20 (34.4%)--spontaneous rupture of the transplant, in 11 (20%)--lymphocele, in 5 (9.1%)--arrosive hemorrhage from the renal transplant artery. The methods of surgical correction of the RAT complications were optimized. Urological complications and spontaneous rupture of the renal allotransplant were revealed most frequently. An acute rejection reaction constitutes the most frequent cause of spontaneous rupture of the renal allotransplant. While the RAT surgical complications occurrence an active surgical tactics is adopted.