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。     

移植肾实质自发性破裂八例报告

报告移植肾实质自发性破裂８例患者的临床资料，复习国内文献报告的１６例并进行讨论。认为：排斥反应是移植肾实质自发性破裂的主要病理基础，外力作用是发生破裂的诱因之一；包膜切开可作为一种预防措施；有效的免疫抑制治疗能减轻移植肾破裂出血的程度；移植肾肾区剧烈疼痛是发生破裂的首发症状。早期诊断，及时探查止血，加强免疫抑制治疗，患者均可获得良好疗效。     

胰肾联合移植中供体切取和修整的技巧

目的:总结胰肾一期联合移植中供体胰十二指肠及肾脏切取及修整的经验。方法:回顾性分析19例胰肾联合移植术中供体胰十二指肠及肾脏切取的方法与移植物的修整技巧。结果:无1例发生移植物损伤。联合移植术后9 d之内18例完全停用外源性胰岛素,空腹血糖正常，尿糖≤（+）。术后2～4 d，血肌酐和尿素氮降至正常。3例出现移植肾脏急性排斥反应，2例发生移植胰腺急性排斥反应，给予甲泼尼龙冲击治疗后恢复正常。1例术后因移植物加速排斥反应，术后11 d切除移植胰、肾。结论:胰肾联合移植手术中，供体胰十二指肠及肾脏的切取及修整是手术成功的重要因素之一。     

胰肾联合移植术后排斥反应分析

目的 探讨预防和逆转胰肾联合移植术后排斥反应的方法。方法 回顾性分析1999年9月～2003年9月17例同种异体胰肾联合移植手术患者的临床资料。全部病例采用口服免疫抑制剂：环孢素A、霉酚酸酯或硫唑嘌呤、激素三联用药。其中2例术前及术后第5天应用抗IL-2R单克隆抗体,3例应用OKT3进行免疫诱导。结果 17例患者中1例发生移植胰腺、肾脏加速性排斥反应．经保守治疗无效,切除移植物;8例发生急性排斥反应,其中单纯肾脏排斥反应6例,同时累及胰腺、肾脏的排斥反应2例,经甲泼尼龙或OKT3治疗后均逆转。结论 胰肾联合移植术后合理应用免疫抑制剂。术前采用综合措施降低高危受者的致敏性,是预防和治疗排斥反应的有效方法。     

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。     

细胞间粘附分子—1和血管细胞粘附分子—1在慢性排斥反应中的 …

为了探讨移植肾慢性排斥反应的发病机制，应用免疫组化技术对１６例肾移植术后发生慢性排斥反应患者的移植肾组织及５例正常肾组织行细胞间粘附分子－１，血管细胞粘附分子－１染色及ＨＥ染色。结果表明ＩＣＡＭ－１，ＶＣＡＭ－１在正常肾脏和慢性排斥反应移植肾脏上的表达分布不同。结果提示，它们在移植肾慢性排斥反应的发生，发展过程中起重要的作用。     

移植肾自发性破裂(附15例报告)

目的：总结移植肾自发性破裂的病因，临床表现，诊治及预防，方法：15例患者中，手术探查12例（9例保留移植肾，用明胶海绵填压或医用粘合胶粘贴联合减压，引流处理，3例切除移植肾），3例保守治疗。结果：移植肾切除3例患者行血液透析维持，手术保留移植肾9例和3例保守治疗患者痊愈出院，其中2例手术保留移植肾患者分别于出院98d和6个月因肺部感染，心衰死亡，其他病例随访3－31个月，平均19个月，肾功能均良好，结论：移植肾自发性破裂发生的确切原因尚未清楚，结合临床症状行B超检查对确诊此症价值较高，及时发现，尽早行内，外科联合处理对于移植肾破裂的治疗是重要的，明胶海绵或医用粘合胶粘贴联合减压，引流是一种有效的治疗方法，另外，预防也是一重要环节。     

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。     

胰肾联合移植的排斥反应

目的探讨胰肾联合移植术后的排斥反应。方法对我院施行的3例胰肾联合移植的病人，采用FK506 MMF Perid Zenapax四联免疫治疗方案，通过床边彩超及Cr、BUN、血糖等来监测移植物的排斥反应。对排斥反应采用激素冲击疗法，对激素不敏感者采用OKT3治疗。结果3例患者中有2例出现排斥反应，其发生率达66％；在出现排斥反应时，首先表现为低热、全身不适，尿量减少，血Cr、BUN升高，彩超示移植物血流阻抗升高，之后才是血糖升高。结论胰肾联合移植中，排斥反应与多种因素有关，移植肾对移植胰具有保护作用，肾脏可以作为监测胰腺排异的窗口，彩超检查可以作为筛选移植物排异反应的手段。     

细胞间粘附分子-1和血管细胞粘附分子-1在慢性排斥反应中的表达

为了探讨移植肾慢性排斥反应的发病机制，应用免疫组化技术（ＡＢＣ法）对１６例肾移植术后发生慢性排斥反应患者的移植肾组织及５例正常肾组织行细胞间粘附分子－１（ＩＣＡＭ－１）、血管细胞粘附分子－１（ＶＣＡＭ－１）染色及ＨＥ染色。结果表明ＩＣＡＭ－１、ＶＣＡＭ－１在正常肾脏和慢性排斥反应移植肾脏上的表达分布不同；结果提示，它们在移植肾慢性排斥反应的发生、发展过程中起重要作用     

单纯捆扎法治疗移植肾自发性实质破裂

目的 介绍一种移植肾白发性实质破裂的实用手术治疗方法.方法 移植肾自发性实质破裂14例.移植肾破裂时肾功能正常1例,急性排斥8例,急性肾小管坏死5例.术中证实14例均为肾实质破裂.破裂伤口1个者10例,2个裂12者4例.14例均以受者组织填塞伤口后,以可吸收肠线单纯捆扎加压止血.结果 14例破裂移植肾均治疗成功.术后伤口感染2例,其中1例因合并严重的粒细胞减少症和肺部感染在术后3周死亡.其余13例肾功能恢复满意,术后4～8周出院.随访0.5～5年,人肾存活良好11例,发生慢性移植物肾病2例.结论 单纯捆扎法是快捷、安全、可靠的移植肾自发性实质破裂的治疗方法.     

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.     

Spontaneous rupture of renal transplants

Spontaneous rupture of transplanted kidneys, although uncommon, requires recognition in view of the increasing number of patients subjected to renal transplantation. The etiologic mechanism of spontaneous rupture and our experience with hyperacute rejection associated with spontaneous rupture are discussed. Immunopathologic aspects of hyperacute rejection are correlated with the clinical course, diagnosis, and treatment of spontaneous rupture of transplanted kidneys.     

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.     

The migration activity of blood leukocytes as an index of the immunologic status of a kidney allograft recipient

A total of 48 patients with chronic renal failure, 42 of them after allotransplantation of cadaveric kidney, were studied for leukocyte spontaneous migration and corresponding alterations in migration activity in the presence of renal antigens reflecting recipient sensitivity towards organospecific renal antigens. High levels of leukocyte spontaneous migrations and renal antigen sensitization were recorded in patients with acute course of renal transplant rejection versus those with no evidence of rejection or the persons with slowly progressing chronic rejection. It was stated that alterations in leukocyte migratory activity, both spontaneous and challenged by presence of renal antigen, could demonstrate the activity of immune processes in a recipient of renal transplant. The findings are of help in answering the question of how long the transplant could exist. Moreover, organospecific renal antigens are considered as possible participants, in line with transplantation antigens, in the mechanism of kidney rejection.     

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.     

Calculus in 16-year-old cadaveric kidney transplant: a unique case and literature review

Calculi are rare in transplanted kidneys with an incidence of 0.1-0.2% of all urological complications. The clinical presentation of an obstructing stone is different from that seen in nontransplant patients and can be easily mistaken for rejection. Ultrasonography and renogram may fail to detect it. Steroid therapy, the treatment of choice for acute rejection, may improve renal functions albeit obstruction. An obstruction ureteral stone in a 16-year-old cadaveric kidney transplant was mistaken for acute rejection. Steroid therapy improved renal function for a short time, but then anuria recurred. Failing treatment, the kidney was considered lost and hemodialysis was started. Spontaneous passage of a stone and improved renal functions clarified the picture. The literature regarding kidney transplant stones is reviewed.     

Role of cold ischemia in acute rejection: characterization of a humoral-like acute rejection in experimental renal transplantation

The aim of the study was to characterize the role of cold ischemia in the process of acute rejection using an experimental renal transplant model. Syngeneic renal transplants were performed between Wistar Agouti rats and allogeneic grafts using Wistar-Agouti rats as recipients of Brown-Norway kidneys. For cold ischemia (CI), kidneys were preserved in Euro-Collins (4 degrees C/ 2.5 hours). Rats were bilaterally nephrectomized at the moment of renal transplant and did not receive any immunosuppressant. The groups were NoAR (n = 6): immediate syngeneic transplant; CI-NoAR (n = 6): syngeneic transplant with CI; AR (n = 13): immediate allogeneic graft; CI-AR (n = 6): allogeneic graft with CI. Allogeneic rats were followed for the survival study. Syngeneic rats, with mean survival time beyond 6 months, were sacrificed on the day 7 to compare grafts with those in the allogeneic groups. H&E- and PAS-stained grafts were evaluated using the Banff criteria. Tissue INF-gamma and TNF-alpha were quantified by RT-real time-PCR on the kidney grafts. Renal insufficiency did not appear in the NoAR group, but it did from the posttransplant day 5 in both acute rejection groups. While NoAR kidneys showed well-conserved renal architecture, then AR group displayed variable degrees of tubular necrosis with scarce cellular infiltration, interstitial hemorrhage, vascular damage with fibrinoid necrosis, perivascular edema, and nuclear disruption. Cold ischemia in rejecting animals increased the mortality rate due to renal insufficiency and accelerated acute rejection. Independently of CI, the proinflammatory cytokines TNF-alpha and INF-gamma were increased in both rejection groups. In conclusion, addition of CI overactivates the acute rejection process via a humoral component.     

Late spontaneous kidney graft decapsulation after administration of sirolimus in a recipient with chronic hepatitis B and C infection: a case report

Late spontaneous kidney graft decapsulation with fluid collection is a rare condition with only a few cases reported in the literature. Common causes of renal allograft rupture include acute rejection, acute tubular necrosis, renal vein thrombosis, and trauma. Sirolimus related late spontaneous decapsulation has not been reported in the past. Interestingly, sirolimus may promote lymphocele formation in renal transplant recipients, including those presenting with chronic hepatitis B or C. Herein, we report a case of late spontaneous decapsulation with subcapsular hematoma formation developing 12 years after receipt of a cadaveric allograft. The patient was infected with both hepatitis B and C viruses. Cyclosporine was replaced by sirolimus for maintenance therapy because of chronic rejection and acute deterioration of renal function. He presented to the hospital at 9 months after sirolimus inception because of a sudden onset of pain and swelling over the kidney graft. Magnetic resonance imaging found the capsule to be stripped from the kidney by a collection of liquefied hematomas. A laparoscopic fenestration was performed by creation of a peritoneal window adjacent to the renal allograft. When patients have chronic hepatitis, tacrolimus might be a better choice than sirolimus.     

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.