抗人类白细胞抗原与抗组织相容性Ⅰ类相关链A位点特异性抗体对移植肾功能的监测价值

目的 探讨抗人类白细胞抗原(HLA)与抗主要组织相容性Ⅰ类相关链A位点(MI-CA)抗体在移植肾功能中的意义.方法 采用免疫磁珠流式液相芯片技术检测135例等待肾移植患者中的抗HLA和抗MICA抗体,其中33例.肾移植患者接受了2年的动态随访;采用PCR-SSOP方法 进行HLA和MICA基因分型并鉴定供者特异性抗体(DSA)和非供者特异性抗体(NDSA),结合血清肌酐水平和临床资料进行分析.结果 34.1%等待肾移植患者(46/135)预存抗HLA和抗MICA抗体.动态随访33例肾移植患者:20例患者移植前后抗体均阴性;10例患者移植前后抗体阳性且类型未改变;3例患者移植6个月后产生新生抗体(9.1%).2例移植前抗体阴性,移植后6个月新生A33、A31和DQ7、DR17、DR18为NDSA抗体,移植后1、2年新生DR12和DR11为DSA抗体;1例移植后1年新增MICA27和MICA02特异性抗体的同时新生HLA-B41、A32抗体.在33例肾移植患者中,抗体阳性组患者与抗体阴性组比较差异有统计学意义(P＜0.05);MICA抗体阳性组患者的血清肌酐水平升高更明显(P＜0.01).结论 无论肾移植前患者是否预存抗HLA和抗MICA抗体,移植后动态监测抗HLA和抗MICA特异性抗体的变化,对预警排斥反应的发生和指导临床治疗来防止移植肾功能减退均具有一定价值.     

肾移植术后供者特异性抗体对移植肾近期效果的影响

目的 评价肾移植术后供者特异性抗体(Ds-Ab)对移植肾近期效果的影响。方法 对2001年1月至2002年7月间进行尸肾移植的92例受者，使用酶联免疫吸附(ELISA)法，检测受者血清中HLA抗体水平，随访1年。结果 16例(17．4％)受者术后出现供者特异性抗体。抗体阳性组急性排斥发生率(56．3％)高于抗体阴性组(11．9％)，P=0．000；移植肾功能延迟恢复的发生率(12．5％)与抗体阴性组(9．2％)比较，差异无显著性，P=0．102；供者特异性抗体阳性组受者发生急性排斥后，移植肾肌酐水平高于抗体阴性组或无急性排斥组。结论 供者特异性抗体与肾移植术后急性排斥有关，可能影响近期移植肾功能。     

供者特异性抗体监测在肾移植中的应用

目的 研究肾移植术后受者血清中供者特异性抗体（DSA）与发生急性排斥反应的关系,为临床早期诊断、合理制定个体化治疗方案、评估疗效提供客观的参考依据.方法 选取2012年1月至2013年8月西安交通大学医学院第一附属医院肾病医院肾移植科285例首次肾移植受者,术后动态监测DSA水平,检测时间点为术后3,5,7,14,21,30,60,90 d.观察受者肾功能和急性排斥反应发生情况.使用卡方检验或Fisher精确概率法比较不同HLA抗体类型的受者急性排斥反应发生率.结果 285例肾移植受者术后初筛人类白细胞抗原（HLA）抗体阳性率为22.11％ （63/285）,其中DSA阳性4例.急性排斥反应发生率6.67％ （19/285）.HLA抗体阴性受者和HLA抗体阳性且DSA阴性受者急性排斥反应发生率分别为3.15％ （7/222）和16.95％ （10/59）,二者相比差异有统计学意义（x2=12.891,P＜0.05）;4例DSA阳性受者有3例发生急性排斥反应,与HLA抗体阴性、HLA抗体阳性且DSA阴性受者急性排斥反应发生率相比,差异均有统计学意义（P=0.000和P=0.016）.19例发生急性排斥反应受者经甲泼尼龙、兔抗人胸腺细胞免疫球蛋白冲击治疗或血浆置换等治疗后,15例受者成功逆转,1例死于并发症.结论 动态监测肾移植术后受者DSA水平,可预测移植肾功能状态,对急性排斥反应的发生有重要预警作用,有利于及时清除或降低DSA水平,对有效预防和及时诊治排斥反应具有重要作用。     

采用流式细胞微珠法检测肾移植受者体内供者特异性抗体39例

目的 应用流式细胞微珠法检测肾移植受者供者特异性抗体(DSA),并探讨DSA阳性受者的HLA配型及移植物排斥反应发生情况.方法 检测39例亲属肾移植受者移植前、后的DSA,检测供、受者HLA错配情况,记录受者移植后排斥反应的发生情况.分析DSA阳性及阴性受者的HLA错配及排斥反应的发生情况.结果 39例共检测DSA 313次,其中移植前78次,移植后235次,移植前出现DSA阳性的均暂缓手术.5例HLA无错配的受者移植后DSA均为阴性,34例HLA错配的受者移植后12例出现DSA阳性(35.3％,P＜0.05).12例DSA阳性受者中,5例发生排斥反应(41.7％),其排斥反应发生率显著高于DSA阴性的移植受者(7.4％,P＜0.05).发生排斥反应且DSA阳性受者的单抗原微珠免疫荧光强度均值为5723.9±1030.5,高于未发生排斥反应的DSA阳性者的2355.2±609.7(P＜0.05).DSA阳性的受者治疗后,DSA免疫荧光强度有所下降.结论 采用流式细胞微珠法动态监测DSA效果较好,有利于预测和及时防治肾移植后排斥反应.     

亲属活体肾移植受者预存抗HLA抗体的处理及临床疗效观察

目的 探讨亲属活体肾移植受者预存抗HLA抗体的处理及效果.方法 移植前预存抗HLA抗体者15例,其中2例为供者特异性抗体(DSA),13例为非供者特异性抗体(NDSA).预存DSA者,术前2周开始每2～3 d行血浆置换1次,共行4～5次,每次血浆置换后静脉输注小剂量免疫球蛋白,移植当天给予利妥昔单抗375 mg/m2.术前10 d起给予他克莫司(Tac,0.1mg· kg-1·d-1)+吗替麦考酚酯(MMF,0.5 g/d).术后静脉注射免疫球蛋白(IVIG)0.2～0.4 g·kg-1·d-1,用2～3 d.预存NDSA者,术前第3天行血浆置换治疗1次,部分病例在血浆置换治疗后每天IVIG 0.6 g/kg.15例受者均采用抗胸腺细胞球蛋白(ATG)+甲泼尼龙进行诱导治疗,免疫抑制维持治疗采用Tac+ MMF+泼尼松.结果 预存DSA者,在去抗体减敏治疗后,群体反应性抗体(PRA)和淋巴细胞毒交叉配合试验(CDC)转为阴性;预存NDSA者,其CDC始终阴性,去抗体减敏治疗后仅有部分患者的PRA有所降低.2例预存DSA的受者分别于术后第14天和1个月时出现急性和交界性体液性排斥反应,抗体反弹,予以血浆置换+大剂量IVIG(1～2 g/kg)后,均能有效控制和逆转.现分别随访1年和10个月,肾功能维持良好.13例预存NDSA的受者,1例发生加速性排斥反应,予ATG治疗后逆转;1例发生急性体液性排斥反应,经大剂量IVIG治疗后逆转;1例发生急性细胞性排斥反应伴慢性化改变,甲泼尼龙冲击治疗的效果不佳,移植肾丧失功能.结论 对于预存DSA的患者,采用血浆置换+IVIG+利妥昔单抗进行去抗体减敏治疗,在其PRA和CDC转阴后再行移植,安全性和短期疗效良好.     

采用单抗原微珠抗体检测肾移植受者体内供者特异性抗体

目的 总结应用单抗原微珠抗体检测肾移植受者体内供者特异性抗体(DSA)的经验,并探讨阳性DSA的处理方法及对移植肾功能的影响.方法 应用流式细胞微珠法检测亲属肾移植受者移植前后单抗原微珠抗体,并分析DSA与排斥反应、移植肾功能的关系.结果 30例患者,检测样本173份,其中移植前47份,移植后126份.移植前1例出现DSA,移植后8例出现DSA,应用硼替佐米及增加免疫抑制剂治疗.应用硼替佐米治疗者1例DSA免疫荧光强度下降至阴性水平,2例下降超过50％.出现DSA时与未出现DSA时的估算肾小球滤过滤分别为(1.50±0.59) ml/s与(1.23±0.38) ml/s,差异有统计学意义(P＜0.05).结论 采用单抗原微珠抗体动态检测DSA的效果好,DSA的出现影响了移植肾eGFR,应用硼替佐米治疗可使DSA免疫荧光滴度下降.     

抗HLA和抗MICA抗体的表达对移植肾功能和急性排斥反应的预示作用

目的 探讨抗HLA与抗主要组织相容性复合物Ⅰ类链相关基因A(MICA)抗体的表达对移植肾功能和急性排斥反应的预示作用.方法 采用免疫磁珠流式液相芯片技术检测41例肾移植受者移植前后的抗HLA和抗MICA抗体,其中37例接受了1、3、6个月及1、2、3年的动态随访.分析抗HLA和抗MICA抗体的特异性,及其与血清肌酐和排斥反应的相关性.结果 移植前共有9例(22.0%,9/41)预存抗HLA或(和)抗MICA抗体,其巾抗HLA抗体阳性2例(4.9%,2/41),抗MICA抗体阳性6例(14.6%,6/41),抗HLA和抗MICA抗体均阳性1例(2.4%,1/41).另外有5例抗MICA抗体可疑阳性.除1例的抗MICA抗体为供者特异性抗体(DSA)外,其余均为非供者特异性抗体(NDSA).37例随访者中,6例新生抗HLA抗体(16.2%),3例新生抗MICA抗体(8.1%),新生抗HLA抗体者的抗体滴度在随访3年中呈现上升趋势.9例预存抗体的受者,有4例(44.4%,4/9)发生排斥反应;6例新生抗HLA抗体的受者中,有3例(50.0%)发生急性排斥反应,而3例新生抗MICA抗体的受者均无排斥反应发生,二者间的差异有统计学意义(P＜0.05).新生抗HLA抗体产生较早(术后3 d和7 d)的2例受者均检测到抗HLAⅡ类DSA,其移植肾均因排斥反应而切除.预存抗MICA抗体,且移植后发生排斥反应者在随访的每个时间点上的血清肌酐水平均高于预存抗MICA抗体但无排斥反应者(P＜0.05);移植前抗HLA和抗MICA抗体均阴性者,术后发生排斥反应者在随访的每个时间点上的血清肌酐水平均高于抗体阴性且无排斥反应者(P＜0.01);无论是新生抗HLA抗体还是抗MICA抗体,移植后1个月发生排斥反应者的血肌酐均明显高于抗体阴性且无排斥反应者(P＜0.01).结论 预存和新生抗HLA抗体是移植后发生急性排斥反应的重要因素,而供、受者HLA和MICA基因错配是产生新生抗体的重要原因.     

移植肾活检组织检测供者HLA四分位基因分型的临床应用

目的明确移植肾活检组织检测的供者HLA四分位基因分型结果的准确性及临床应用。方法回顾性分析2019—2022年在西安交通大学第一附属医院进行肾移植后随访的受者资料, 对可疑排斥反应但缺乏供肾HLA四分位基因分型的38例肾移植受者进行移植肾穿刺, 提取移植肾穿刺组织DNA, 采用LABType SSO法, 进行HLA四分位基因分型检测, 与受者已知HLA基因型进行比对, 预测供者HLA基因型。采用Labscreen Single试剂盒进行供者特异性抗体(DSA)检测, 对38例肾移植的供、受者的临床基线资料、HLA分型资料、受者DSA抗体数据、移植肾病理学指标等进行统计分析。结果 38例受者中, 12例(31.58%)HLA-A、B、C、DR、DQ位点全部检测出;14例(36.84%)检出4个位点;10例(26.32%)检出3个位点;2例(5.26%)检出2个位点, 检出位点和移植时间存在负相关关系(rs=-0.707, P=0.001)。HLA位点检出率分别为A:78.94%(30例);B:65.78%(25例);C:84.21%(32例);DR:57.89%(22例);DQ:100%...     

肾移植术后特异性HLA抗体对急性排斥的影响

目的评价肾移植术后特异性HLA抗体对移植肾急性排斥的影响.方法采用前瞻性队列研究,通过酶联免疫吸附(ELISA)法检测136例肾移植患者围手术期特异性HLA抗体水平,随访观察HLA抗体对急性排斥的影响.结果术后HLA抗体阳性组急性排斥发生率高于阴性组(32.65%vs13.79%,P=0.000).按照HLA-Ⅰ类和Ⅱ类抗体水平分组后,移植肾无排斥存活率依次为HLA-Ⅰ-/Ⅱ-组＞HLA-Ⅰ-/Ⅱ+组＞HLA-Ⅰ+/Ⅱ-组＞HLA-Ⅰ+/Ⅱ+组(P=0.03).结论术后特异性HLA抗体可能是引起移植肾急性排斥的原因之一,HLA-Ⅰ类抗体与急性排斥关系较为密切.     

人类白细胞抗原配型对移植肾失功患者群体反应性抗体产生的影响

目的 探讨人类白细胞抗原(HLA)配型对移植肾失功患者群体反应性抗体(PRA)产生的影响. 方法对24例术前PRA阴性的初次肾移植病例行供受者HLA分型,移植.肾失功后检测受者PRA并确定抗体特异性.PRA定性、定量及确定抗体特异性用莱姆德混合抗原板(LATM)及莱姆德抗原板1240(LAT1240)检测.HLAI类及Ⅱ类抗原分型用顺序特异引物聚合酶链反应(PCR-SSP)技术.观察PRA产生情况,比较致敏与非致敏病例的HLA配型情况,并分析HLA错配与PRA产生的关系.结果 24例中PRA阳性17例,阴性7例.17例致敏患者中Ⅰ类抗体阳性8例,Ⅱ类抗体阳性15例,Ⅰ类及Ⅱ类抗体同时阳性6例.A1(3例)、A24(2例)、DR7(6例)、DR9(4例)、DRl2(3例)及DRl3(4例)抗体多见,供者特异性抗体(DSA)中A1(2例)、DR7(4例)及DR9(3例)多见.按6抗原配型标准比较Ⅰ类抗原错配数,Ⅰ类抗体阳性组(8例)与阴性组(16例)问比较差异无统计学意义(P＞0.05),按交叉反应组(CREG)配型标准阳性组错配数多于阴性组(P＜0.01);比较Ⅱ类抗原错配数,Ⅱ类抗体阳性组(15例)错配数多于阴性组(9例)(按6抗原配型标准P＜0.05,按CREG配型标准P＜0.01).供者HLA频率及错配频率最高的A2及A30未发现相应抗体产生,供者A1-受者A2、DR7及DR9错配易导致DSA产生.结论 HLA错配是移植肾失功患者致敏的重要原因.供者抗原出现频率及错配频率与PRA及DSA出现频率不完全一致,某些抗原错配更易导致PRA及DSA产生.初次肾移植良好的HLA配型可减少等待再次肾移植患者的致敏发生率.     

动态分析HLA和MICA特异性抗体对移植肾功能的影响

目的 探讨肾移植前后人类白细胞抗原(HLA)和主要组织相容性一类相关链A基因(MICA)抗体特异性对移植后排斥反应和移植肾功能的影响. 方法采用免疫荧光液相芯片技术检测27例肾移植(尸供22例,亲属活体供肾5例)受者手术前后抗HLA抗体和MICA抗体的特异性和阳性值变化,并结合供受者的基因分型,区分供体特异性抗体和非供体特异性抗体.取同期的临床资料和SCr水平进行分析. 结果 27例移植患者中带肾存活26例,移植肾失功1例.移植后1、3、6、12个月时动态随访24例,失访2例.27例患者移植前预存抗体7例(25.9%),其中HLA抗体阳性2例、MICA抗体阳性3例,HLA和MICA抗体均阳性2例.肾移植前HLA和MICA抗体均阴性者中移植后3～6个月产生新生抗体3例.1例新生HLA-Ⅱ类特异性抗体者,移植半年后出现慢性排斥反应,经治疗术后1年SCr>200 btmol/L.3例肾移植前MICA抗体阳性者,术后MICA抗体的特异性均无改变,但抗体的阳性分值呈现2～8分的变化,1年后均升高到移植前(4～8分)水平.移植前预存低阳性率HLA-Ⅱ类特异性抗体者1例,移植后2周有发热等排斥反应,巨细胞病毒检测阳性,移植后1个月时SCr为171μmol/L,3个月升高到236μmol/L.24例分为抗体阴性组(14例)和抗体阳性组(10例).移植后1个月和1年时SCr水平2组间比较差异有统计学意义(P=0.03,0.05). 结论 移植后3～6个月是新生抗体变化的重要随访时间,可根据HLA和MICA抗体的特异性和阳性分值变化,尽早采取有效方法预防排斥反应和减少移植肾功能减退的发生和发展.     

Development of Nondonor-Specific HLA-DR Antibodies in Allograft Recipients Is Associated with Shared Epitopes with Mismatched Donor DR Antigens

Our previous studies showed that not only donor-specific antibodies (DSA) but also nondonor-specific antibodies (NDSA) were detected in the peripheral blood of allograft recipients. The molecular mechanism involved in the development of NDSA is examined here. HLA class II single antigen (SA) beads were used to determine the presence of HLA DR-specific antibodies in renal transplant recipients with failed allografts. Sequence-based antibody-epitope mapping was determined by the comparison of the reaction profiles of different SA recombinant cell lines containing unique epitope pattern. We found that 22 out of 65 recipients with failed grafts developed antibodies against donor HLA DR that is a mismatch with the recipient. Three of them had only DSA while 19 patients had not only DSA but also NDSA. An average of 77.3% of NDSA reacted with targets that share amino acid sequence with mismatched donor DR antigens. Either surface or nonsurface amino acid residues may constitute an antibody epitope. In conclusion, development of NDSA in allograft recipients may be associated with shared amino acids with mismatched donor antigens. SA beads technique not only helps to determine antibody specificities but also provides an ideal approach for the identification of potential HLA antibody epitopes.     

The presence of donor-specific antibodies in renal transplantation

Determining the presence of anti-HLA antibodies before transplantation is an important factor to prevent loss of function among renal transplantations. In addition, recent studies have shown that not only the pretransplantation existence of anti-HLA antibody but also posttransplantation donor-specific antibodies (DSA) and non-donor-specific antibodies are significantly associated with allograft rejection or loss of graft function. This study presented DSA among patients after renal transplantation together with graft function and survival.     

Effect of posttransplant anti-HLA antibody on outcome of renal transplantation

Pretransplant anti-HLA antibody has an impact on renal transplantation (RT) outcome. However, the role of posttransplant anti-HLA antibody in renal allograft outcome remains unclear. We conducted this study to determine whether posttransplant anti-HLA plays an important role in the outcome of renal allografts. Our investigation used a cross sectional design. Class I and II anti-HLA antibodies were obtained in 41 renal transplant patients. Patients had undergone either living-related (n = 15) or cadaveric (n = 26) RT. All patients had been transplanted for >6 months. The correlation of posttransplant class I and class II, anti-HLA antibodies with renal allograft function glomerular filtration rate (GFR) was analyzed. Patients displaying a GFR of >60 mL/min showed positive anti-HLA antibody status for class I (n = 2) and class II (n = 9). In contrast, those whose renal transplants showed a GFR <60 mL/min included three patients positive for HLA class I and 19 patients for HLA class II. Posttransplant class II anti-HLA antibody showed a negative correlation with GFR (r = -0.31, P = .03). Preliminary results indicated that class II posttransplant anti-HLA antibody might be one mechanism of chronic renal allograft rejection and may confirm the important role of HLA matching in renal transplantation outcome.     

Development of posttransplant antidonor HLA antibodies is associated with acute humoral rejection and early graft dysfunction

BACKGROUND: The goal of this study was to determine whether the production of posttransplant antibodies directed against donor HLA mismatches (donor specific antibody; DSA) is associated with renal allograft rejection and early graft dysfunction. METHODS: Forty-nine adult renal allograft recipients with increased risk of rejection were enrolled during the period of October 2001 through May 2003 and were prospectively monitored for the development of anti-HLA antibodies. RESULTS: Of 49 patients, eight (16.3 %) patients were diagnosed with acute humoral rejection (AHR) and 11/49 (22.4%) patients were diagnosed with acute cellular rejection (ACR). A strong association between pretransplant HLA sensitization and AHR was found (P=0.005). Of the eight patients diagnosed with AHR, the majority developed DSA before or concomitant with episodes of rejection (P<0.001). Only 3 of 41 patients (7.3%) without AHR developed DSA. The pathogenic role of alloantibodies was further substantiated by analyzing their association with graft function as measured by serum creatinine levels. The average serum creatinine after the third month posttransplantation in DSA producers was 2.24+/-1.01 mg/dL, while in non-DSA patients the average serum creatinine was 1.41+/-0.37 mg/dL (P<0.01). CONCLUSION: This study reveals a strong association between the production of DSA, AHR, and early graft dysfunction. Our findings indicate that prospective monitoring for anti-HLA antibodies following transplantation is a useful test for the diagnosis and classification of AHR for identifying patients at risk of early graft dysfunction.     

Significance of HLA-matching and anti-HLA antibodies in heart transplant patients receiving induction therapy?

ObjectivesThough Human Leukocyte Antigen (HLA) matching benefits are demonstrated in renal transplantation, evidence in heart transplantation is lacking, and its clinical feasibility is uncertain. Post-transplantation anti-HLA antibodies are being increasingly studied in organ transplantation, with diverging conclusions between transplantated organs.MethodsWe analyzed retrospectively the influence of HLA matching and anti-HLA antibodies on overall survival, acute rejection and chronic allograft vasculopathy in 309 patients receiving induction therapy and triple-drug immunosuppression.ResultsThe average number of HLA-A/B/DR mismatches between donor and recipient was 4.9 ± 1. The majority of mismatches was for Class I HLA-A/B with an average of 3.3, then for Class I HLA-DR with an average of 1.6. Overall, the HLA-A/-B/-DR mismatches had no influence on the cardiac allograft survival (p = 0.28). However, HLA-DR mismatches were negatively correlated to severe cellular and/or humoral allograft rejection (p = 0.04). Our analysis found anti-HLA antibodies in 27% of recipients, de novo anti-HLA antibodies in 16% of recipients, and donor-specific anti-HLA (DSA) antibodies in 8% of recipients. Furthermore, de novo DSA had no influence on the 5-year survival (78% with DSA vs. 92% without DSA; p = 0.49), which may be masked by the limited number of recipients in analysis By univariable analysis, anti-HLA antibodies (preexisting or de novo) unrelated or related to the donor had no influence on severe cellular and/or humoral rejection or on chronic allograft vasculopathy.ConclusionsHLA-DR mismatch was negatively correlated to severe cellular and/or humoral allograft rejection but had no influence on cardiac allograft survival. In this study, anti-HLA antibodies (preexisting or de novo) unrelated or related to the donor had no influence on cellular and/or humoral rejection or on chronic allograft vasculopathy. The results of this study add to the controversy on the impact of allo-antibodies in heart transplant recipients receiving induction therapy and contemporary immunosuppression.     

Control of antidonor antibody production with tacrolimus and mycophenolate mofetil in renal allograft recipients with chronic rejection

BACKGROUND: In renal transplantation, chronic rejection is a major cause of late allograft loss. Recent studies indicate that a subset of chronic rejection is associated with anti-HLA donor specific antibodies (DSA) and complement C4d deposition in peritubular capillaries (PTC). Since rescue therapy with tacrolimus and mycophenolate mofetil has been found to limit antidonor B-cell responses in recipients with acute humoral rejection, we sought to determine whether a similar immunosuppressive regimen might be effective in patients with 'chronic humoral rejection'. METHODS: Four renal allograft recipients with 'chronic humoral rejection' were prospectively identified. The diagnosis was based on: (1) progressive rise in serum creatinine over 12 months; (2) typical pathologic features by light microscopy (transplant arteriopathy and glomerulopathy); (3) widespread C4d deposits in PTC by immunofluorescence; (4) detection of 'de novo' DSA at the time of biopsy. Maintenance immunosuppression was CsA, prednisone and azathioprine (n=3) or prednisone and azathioprine (n=1). Rescue therapy with tacrolimus and mycophenolate mofetil was initiated in all patients, 12 hr after cyclosporine and azathioprine discontinuation. RESULTS: At diagnosis, the mean serum creatinine was 3.9 mg/dl (range: 3.3 to 5.4 mg/dl). DSA was an IgG directed against HLA class II (n=3) or class I (n=2), that is one patient had both anti-HLA class I and class II antibodies. Pretreatment antibody titers varied between 1:8 and 1:128. Rescue therapy was associated with a rapid and sustained decrease in antibody titers. In two patients, DSA became undetectable after 9 months and a repeat biopsy performed after 12 months revealed a decrease in C4d deposition in PTC. CONCLUSION: These results suggest that a decrease in DSA production can be induced in renal allograft recipients with 'chronic humoral rejection' by using an immunosuppressive regimen that combines tacrolimus and mycophenolate mofetil. Limitation of antidonor antibody synthesis may be important for the treatment or the prevention of chronic rejection in organ transplantation.