双滤过法血交分离治疗移植肾术后排斥反应及术前高度致敏

目的 探讨肾移植术后排斥反应和术前高度致敏的治疗方法。方法 采用双滤过法血浆分离术（ＤＦＰＰ）治疗３６例术后排斥反应和９例术前高度致敏患者。结果 ２４例急性排斥中２２例逆转，１０例加速性排斥（ＡＣＲ）全部逆转１例慢性排斥肾功能稳定，１例超急性排斥（ＨＡＲ）摘除移植肾；排斥反应采用ＤＦＰＰ治疗其一年移植肾生存率为８４．０％。去致敏抗体者８例已接受肾移植其中１例术后发生ＨＡＲ。结论认为ＤＦＰＰ是治疗排     

移植肾慢性排斥的研究进展

移植肾慢性排斥的问题日益突出，其发病机理上前还不清楚。本文将对此领域相关的研究进展，学说予以简述。     

应用ALG治疗CsA及激素无法挽回的移植肾难治性排斥

1990年1月至1991年12月采用ALG治疗18例因使用CsA及激素无效的移植肾排斥，结果14例完全逆转（77．7％），1例肾功能不全，2例无效，1例死于肺部感染。     

移植肾急性排斥反应早期无创诊断研究进展

肾移植是当今治疗终末期肾病最有效的手段之一.移植肾急性排斥反应仍是术后主要并发症之一,也是导致后期移植肾慢性失功能的危险因素,因此及早、正确诊断,及时、有效治疗是降低移植术后急性排斥发生率,保证人/肾长期存活的有效手段,在临床工作中有重要的意义.本文从影像学检查、T淋巴细胞亚群、细胞因子变化、基因多态性及代谢组学等方面的研究进行综述.     

体液介导的移植肾排斥

抗体介导（体液介导）的移植肾排斥近年引起广泛关注,相关的理论与临床研究革命性地改变了长期以来人们对移植肾排斥的理解,也为临床上判定预后、预防和治疗提供依据.本文就近年来有关移植肾体液性排斥反应的病原、病因、基本病理变化及其防治方面的研究状况作一概述.     

彩色多普勒超声诊断早期移植肾急性排斥

目的探讨彩色多普勒超声图像数据分析在诊断早期移植肾急性排斥中的作用及临床价值.方法总结203例肾移植术后6～30d内行彩色多普勒超声检查,结合临床症状、生化检查并参照病理诊断,对二维灰阶图像、彩色血流图、血流频谱及阻力指数(RI)、搏动指数(PI)、收缩期与舒张期血流速度比(S/D)等参数进行回顾性分析.结果以彩色多普勒RI>0.78、PI>1.82、S/D>4.1为标准,结合彩色血流图及血流频谱形态,早期移植肾急性排斥正确诊断率可达85.7%.结论应用彩色多普勒超声诊断移植肾早期急性排斥并监测其功能恢复,具有快速、准确、无创等优点,可提早发现病情变化并指导治疗,提高移植肾存活率.     

国产T细胞单克隆抗体WuT3治疗移植肾急性排斥反应

1 临床资料 1998-06/2000-12我们应用WuT3治疗移植肾难治性急性排斥反应39例 男32例,女7例,年龄23～56岁,其中4例为再次肾移植,其余均为首次肾移植。淋巴细胞毒试验(LMC)1％～5％,ABO血型相容,排斤反应发生在3～35 d。肾移植术中用甲基强的松龙(MP)1g,术后1d,2d     

移植肾血管慢性排斥的机理研究

肾移植术的近期疗效已取得显著效果，但其远期效果仍不理想。近年来的研究结果表明肾血管的慢性排斥是其重要原因，移植肾血管阻塞是导致移植肾慢性失功，移植肾丧失的主要障碍。本文将对这方面的研究结果及其进展予以简要综述。     

体液介导的移植肾排斥

抗体介导(体液介导)的移植肾排斥近年引起广泛关注,相关的理论与临床研究革命性地改变了长期以来人们对移植肾排斥的理解,也为临床上判定预后、预防和治疗提供依据。本文就近年来有关移植肾体液性排斥反应的病原、病因、基本病理变化及其防治方面的研究状况作一概述。     

肾移植超急性排斥反应13例次分析

报告１９７８年８月￣１９９４年１２月间共做尸体肾移植５７０例次，其中发生超急性排斥反应（ＨＡＲ）１１例１３例（１３例次），均经病理证实，发生率为２．３％。移植肾于术中或术后短期予以摘除。并结合临床资料对ＨＡＲ的发生机理、危险因素、鉴别诊断及预防等进行分析，认为ＨＡＲ的发生与受者体内的预存抗体有关，反复输血、多次妊娠、再次肾移植是ＨＡＲ的诱发因素，术前系统、准确的配型有助于减少ＨＡＲ的发生。     

Roles of vascular endothelial growth factor in acute rejection reaction following liver transplantation

The presently known cytokines that participate in acute rejection of organ transplantation include four categories by order of function: inflammatory cytokines, immunospecific cytokines, inflammatory cell activating cytokines and growth cytokines. Of them, growth cytokines that directly induce division, proliferation and migration of endothelial cells mainly include the vascular endothelial growth factor (VEGF) family and the fibroblast growth factor (FGF) family [1]. Recent studies [2] showed that interactions and time overlap of inflammatory cell infiltration and angiogenesis are the main mechanisms that induce acute rejection (AR) following organ transplantation, which has been demonstrated by the clinical fact that AR symptoms after liver transplantation could only be relieved by combination use of drugs for improving micro vessels and those for improving micro bile ducts. This article is a review of VEGF that mediates inflammatory cell infiltration and angiogenesis in the portal area [3].     

Completely reversed acute rejection is not a significant risk factor for the development of chronic rejection in renal allograft recipients

Although acute rejection (AR) has been shown to correlate with decreased long-term renal allograft survival, we have noted AR in recipients who subsequently had stable function for more than 5 years. We reviewed 109 renal graft recipients with a minimum of 1 year graft survival and follow-up of 5–8 years. Post-transplant sodium iothalamate clearances (IoCl) measured at 3 months and yearly thereafter were used to separate recipients into 2 groups. In 61 patients (stable group), there was no significant decrease ( > 20 % reduction in IoCl over 2 consecutive years) in IoCl. Forty-eight patients had significant declines in IoCl (decline group). Groups were compared for incidence, severity, timing, and completeness of reversal of AR. Rejection was considered completely reversed if the post-AR serum creatinine (Scr) returned to or below the pre-AR nadir Scr after antirejection therapy. The incidence of AR was not significantly different between groups (47 % vs 52 %). A trend toward a lower mean number of AR episodes per patient was noted in the stable group (0.69 vs 1.04, P = 0.096), but the timing of AR was not different. Steroid-resistant AR occurred in approximately 25 % of both groups. A striking difference was seen in complete reversal of AR, with the stable group having 100 % (42/42 episodes of AR in 29 patients) complete reversal whereas only 32 % (8/25) of the patients in the decline group had complete reversal (P < < 0.001). Of 8 declining patients with complete reversal, graft loss was due to chronic rejection (CR) in only 3. Seventeen declining patients had incomplete reversal of AR, and 82 % (14/17) lost their grafts to CR. Overall, only 8 % (3/37) of the recipients with complete reversal of AR developed CR. No patients with incompletely reversed AR had stable long-term function as measured by IoCl. AR is not invariably deleterious to long-term renal graft function if each episode of AR can be completely reversed. Received: 9 March 1999/Revised: 28 December 2000/Accepted: 11 April 2000     

Tacrolimus rescue therapy for children with acute renal transplant rejection

Seventeen children with renal transplants (11 living-related, age 2–18 years) were converted from cyclosporine to tacrolimus because of acute rejection that failed to respond to high-dose corticosteroids. Resistance to corticosteroids was confirmed by renal biopsy in 14 patients, and assumed in 3 patients because of failure of serum creatinine to improve to baseline values. Four patients were also treated with OKT3, and 15 children had been receiving mycophenolate maintenance therapy prior to conversion to tacrolimus. Rejection occurred at 2–174 weeks post transplant (mean 52 weeks). Actuarial 1- and 2-year graft survival was 87% and 78%. Three children progressed to end-stage renal disease after 4, 12, and 13 months of tacrolimus. The remaining 14 children have functioning allografts after 20–168 weeks of treatment (mean 80 weeks). All 14 children exhibit stable or improved renal function: serum creatinine 1.1±0.7 mg/dl versus 2.0±0.9 mg/dl prior to tacrolimus. In conclusion, tacrolimus was effective therapy for both early and late acute rejection in children who failed to respond to high-dose corticosteroids. No significant short-term adverse effects were encountered. Received: 29 August 2000 / Revised: 31 July 2001 / Accepted: 31 July 2001     

供体骨髓输注发生嵌合体与肾移植急性排斥反应的关系

目的：探讨供体骨髓输注发生嵌合体与肾移植急性排斥反应的关系及其临床意义.方法：将供体为男性的女性尸体肾移植患者55例,分为术前未行供体骨髓输注者30例（未输注组）;术前行供体骨髓输注的肾移植25例（输注组）.自末梢血中提取DNA,利用nested PCR法检测Y染色体上的特异基因片断DYZ-1.结果：证实有微嵌合发生共32例中13例（40.6%）、23例无嵌合体存的病例中有10例（43.5%）,都发生过1次或1次以上的急性排斥反应,两组之间比较差异无统计学意义;输注组中当微嵌合现象消失、PCR检测转为阴性时,未见排斥反应病例发生.结论：供体骨髓输注有利于促进微嵌合的形成,嵌合体的消失现象与急性排斥反应之间无相关关系,不能以此作为诊断急性排斥反应的依据.     

Single centre experience with mycophenolate mofetil for refractory rejection in cadaveric renal transplantation

Ten patients with refractory rejection following renal transplantation were treated with mycophenolate mofetil (MMF) in an attempt to salvage the allografts. All cases of rejection were biopsy-proven. Seven of the patients had initially been on tacrolimus-based triple therapy and three were on cyclosporin-based regimens. Those on cyclosporin had been unsuccessfully converted to tacrolimus prior to receiving MMF. All patients had received at least one course of methylprednisolone pulse therapy and three had been given OKT3 prior to MMF. MMF was prescribed at a dose of 2000 mg per day in two divided doses and was given in addition to tacrolimus and prednisolone. Eight of the ten patients showed evidence of reversal of rejection, as indicated by improvement in renal function following commencement on MMF, whilst two patients experienced ongoing rejection and underwent graft nephrectomy. One of the patients successfully treated has since had his MMF discontinued due to gastrointestinal intolerance. We conclude that MMF is effective in salvaging renal allografts with resistant rejection and that it has an acceptable side-effect profile. Received: 30 September 1997 Received after revision: 2 December 1997 Accepted: 14 January 1998     

ABO血型基因与移植肾急性排斥反应相关性的研究

目的 探讨ABO血型基因与移植肾急性排斥反应(AR)的相关性.方法 采用引物特异性聚合酶链式反应(PCR-SSP)技术检测2009年5月至2010年2月87例肾移植受者及其对应的48例供者ABO(A1、A2、B、O1、O2)血型基因,分析供受者ABO血型基因相合组与错配组受者AR发生、治疗及转归情况.结果 PCR-SSP测定ABO血型基因推定的表型和血清学方法测定ABO血型表型完全相符.供受者ABO血型基因相合组受者50例,发生AR 6例,经甲泼尼龙(MP)冲击治疗后临床逆转.ABO血型基因错配组受者37例,发生AR 11例,经MP冲击治疗后,临床逆转10例,周期性反复发生AR 1例.错配组与相合组受者AR发生率差异有统计学意义(29.7%与12.0%,P<0.05).错配组1例A2O1血型基因受者接受A1O1血型基因供肾后,受者血清检测发现抗A1抗体,抗体效价IgG 1:64,IgM 1:16,移植术后3～10个月周期性反复发生AR,且周期逐渐变短,激素疗效逐渐降低,术后1年SCr达441μmol/L.结论 检测供受者HLA时同步检测ABO血型基因具有很强的可行性.A2血型基因受者适宜选择O型供肾.供受者ABO血型基因错配是介导肾移植术后AR的危险因素,检测供受者ABO血型基因,降低ABO血型基因错配率对预防AR有一定的临床意义.     

肿瘤坏死因子α基因启动子多态性与肾移植术后急性排斥反应的关系

目的　探讨肿瘤坏死因子α(TNF α)基因启动子 3 0 8位多态性在预测肾移植术后急性排斥反应中的意义。　方法　酶联免疫吸附试验检测 3 5例肾移植患者术前外周血细胞分泌的TNF α水平 ,应用限制性片段长度多态性 (PCR RFLP)方法检测TNF α基因启动子 3 0 8位多态性 ,分析其与术后急性排斥反应的关系。　结果　TNF α启动子 3 0 8位为A/A、A/G基因型者TNF α水平分别为(62 4.96± 177.78)pg/ml、(5 44 .3 2± 13 2 .42 )pg/ml,明显高于G/G基因型者的 (2 3 3 .16± 2 5 .3 7)pg/ml,P<0 .0 1。在HLA DR错配情况下 ,TNF α高分泌基因型受者有 5例 (5 0 % )术后发生急性排斥反应 ,而低分泌基因型受者仅有 2例 (8% )发生急性排斥反应 (P =0 .0 12 )。　结论　肾移植受者TNF α基因启动子 3 0 8位多态性与体外细胞因子产生水平有关 ,TNF α高分泌基因型是术后 3个月内发生急性排斥反应的高危因素     

术前巨细胞病毒感染对移植肾急性排斥的影响

目的 研究肾移植受者术前巨细胞病毒(CMV)感染对术后急性排斥的影响及预防性抗病毒治疗的意义。方法 回顾性分析416例肾移植受者的术前巨细胞病毒感染，预防性抗病毒治疗和急性排斥的发生情况，并用Logistic回归分析各因素对急性排斥的影响。术前感染受者根据有无预防性抗病毒治疗分为治疗组和非治疗组，比较两组间急性排斥发生率。结果术前巨细胞病毒感染组的急性排斥率显著高于非感染组(29．9％比19．5％，P=0．014)，术前感染受者发生急性排斥的风险增高将近1倍。预防性抗病毒治疗能降低术后CMV疾病的发生率但对急性排斥无影响。结论术前巨细胞病毒感染是术后急性排斥独立的危险因子。常规的预防性抗病毒治疗并不能减少由感染介导的免疫损伤而导致的急性排斥的发生。     

The effect of acute rejection on long-term renal graft survival is mainly related to initial renal damage

Abstract It has been suggested that poor long-term prognosis of acute rejection is due to hyperfiltrationmediated injury secondary to the initial renal damage, rather than to ongoing immunological mechanisms. A total of 953 renal transplant recipients was reviewed to examine the effect of acute rejection episodes on graft function and survival; 40 % had no rejections, 45 % one, 12% two and 3% three. Rejection episodes adversely affected short- and long-term prognosis (5-year survival for no rejections, 62 %; one, 34 %; two, 26 %; three, 19 %, P <0.001) and creatinine clearance at one year (cl 1) (none, 56.7 ml/ min; one, 51.1; two, 52.9; three, 35.2, P < 0.01). This was mainly due to increased graft loss, but patient survival was also reduced (5-year survival for no rejections, 77 %; one, 76 %; two, 63 %; three, 53 %, P < 0.05). There was no overall effect of rejection number, independently of cl 1. However, subgroup analysis showed a detrimental effect of rejection number on grafts with high residual function, i.e. cl 1 > 60 ml/min (5-year graft survival none and one, 87 %; two and three, 71 %, P < 0.01). Late initial rejection episodes adversely affected prognosis (5-year survival 1–7 days, 34 %; 8–60, 31 %; 60–300, 21 %, P < 0.05) and residual graft function (cl 1 1–7 days, 56.2 ml/min; 8–60, 48.7; 60–300, 44.6, P < 0.01). In conclusion, the poor long-term prognostic effect of rejection episodes is mainly, but not entirely, related to initial graft destruction. Late (>2 months after transplantation) initial rejection is an important independent risk factor for graft loss.