肾移植早期尿淋巴细胞表型分析的应用价值

目的：探讨尿淋巴细胞表型分析在肾移植早期免疫监测中的临床应用价值。方法：以流式细胞技术对37例肾脏移植患者的105份尿样本进行尿淋巴细胞表型分析,测定CD3、CD4、CD8、CD19、CD25、HLA－DR阳性细胞百分率,其结果在急性排斥反应组和肾功能稳定组之间进行比较。结果：与肾功能稳定组比较,急性排斥反应组尿淋巴细胞表达HLA－DR数增多非常显著（P＜0．01）,CD8和CD25细胞增多显著（P＜0．05）,而CD3、CD4、CD19细胞数变化不显著（P＞0．05）。在诊断移植肾急性排斥反应上,HLA－DR阳性样本的诊断敏感性和特异性分别达86．96％和90．24％,CD8和CD25阳性标本的阴性预测值分别达86．79％和85．71％。结论：尿淋巴细胞表型分析可间接反映出移植肾内的免疫状态,是诊断和鉴别诊断移植肾急性排斥反应的有效方法,适用于肾移植早期的免疫监测。     

CD44分子在肾移植患者急性排斥反应肾组织中的表达及意义

目的:探讨CD44分子与肾移植急性排斥反应的关系。方法:回顾分析2005年7月～2009年5月间肾移植术后穿刺病理活检证实为急性排斥反应患者28例的CD44在移植肾组织中的表达。结果:28例急性排斥反应肾组织中有25例CD44呈阳性表达,阳性率为89.29%;10例慢性排斥反应肾组织中有3例阳性表达,阳性率为30%;30例正常肾脏组织中5例CD44分子的阳性表达,阳性率为16.7%;两两比较,结果差异有统计学意义(P0.05)。结论:CD44与其与配体的相互作用在移植肾急性排斥反应中可能起到重要作用,CD44分子有可能成为一个特异性和敏感性都较好的早期诊断急性排斥的预测因子。     

CD44在大鼠肾移植急性排斥反应中的表达

目的:探讨移植肾组织CD44的表达及血清中可溶性CD44的含量与急性排斥反应的关系。方法:雄性Wistar大鼠和SD大鼠分别作为供体和受体,共分为四组,采用改进的Blom法大鼠原位肾移植模型。免疫组织化学染色法检测移植肾组织CD44分子的表达;酶联免疫吸附试验测定术后血清中可溶性CD44水平的变化。结果:移植肾组织CD44分子的表达在同种异体移植组显著高于同品系移植组、手术对照组及药物治疗组(均P<0.05);移植肾组织CD44分子的表达与急性排斥反应呈正相关(皮质:r=0.734,髓质:r=0.670,均P<0.01);发生急性排斥反应的移植肾组织CD44分子的表达与Banff急性排斥反应指数无相关性(P>0.05);血清中可溶性CD44分子各组间差异无统计学意义,与急性排斥反应及Banff指数均无相关性(均P>0.05)。结论:CD44分子在肾移植急性排斥反应的发病机制中起着重要作用,为进一步提高移植排斥反应防治水平提供理论依据。     

肾移植患者外周血CD4^＋CD25^＋调节性T细胞的变化及临床意义

目的观察肾移植患者外周血中CD4^＋CD25^＋调节性T细胞水平的变化，探讨其在诊断移植肾急性排斥反应中的作用。方法采用流式细胞仪检测26例肾移植患者及30例正常对照组外周血中CD4^＋CD25^＋调节性T细胞水平。结果①慢性肾衰竭患者外周血CD4^＋CD25^＋调节性T细胞水平与对照组比较，差异有统计学意义（P〈0．05）。②非排斥组移植后1、2、4、8周CD4^＋CD25^＋调节性T细胞水平明显高于移植前（P〈0．01）。③急性排斥组排斥反应主要发生在术后第7～21d，其CD4^＋CD25^＋调节性T细胞水平明显低于同期的非排斥组（P〈0．01）。结论CD4^＋CD25^＋调节性T细胞水平的测定可以作为肾移植患者移植后急性排斥反应诊断和预测预后的重要指标。     

尿流式细胞学在诊断移植肾急性排斥反应中的应用价值

目的：探讨尿流式细胞学在诊断移植肾急性排斥反应中的临床应用价值。方法：对43例肾移植受者的116份尿样本进行尿流式细胞学分析，并将急性排斥组和肾功能稳定组的分析结果进行比较。结果：急性排斥反应组尿淋巴细胞总数以及HLA－DR^ 淋巴细胞数显著增多，与肾功能稳定组比较，P＜0．01，CD8^ 细胞亦增多（P＜0．05），而CD3^ ,CD4^ ,CD19^ 细胞数变化两组差异不显著（P＞0．05），在诊断移植肾急性排斥反应上，HLA－DR阳性样本和淋巴细胞数阳性样本的诊断敏感性和特异性分别达95．2％，90．5％，和92．6％，87．4％，结论：尿流式细胞学分析可反映移植肾内的免疫状态，尿淋巴细胞数的显著增多和尿HLA－DR^ 淋巴细胞增多可以作为诊断急性排斥反应的有意义指标。     

血清及尿白细胞介素-6检测在肾移植中的意义

目的探讨血、尿ＩＬ－６检测在肾移植急性排斥（ＡＲ）诊断及鉴别诊断中的作用。方法应用ＥＬＩＳＡ技术，分别对肾移植术后不同状态下患者血、尿ＩＬ－６水平进行检测。结果急性排斥及感染患者血ＩＬ－６水平较环孢素（ＣｓＡ）中毒、急性肾小管坏死（ＡＴＮ）、移植肾功能正常及正常对照组高。尿ＩＬ－６在急性排斥及感染组也较ＣｓＡ中毒、ＡＴＮ、移植肾功能正常组有明显升高，而急性排斥组较感染组升高更明显。结论血、尿ＩＬ－６水平的升高可作为判断肾移植急性排斥的指标之一；也可作为鉴别急性排斥反应与ＣｓＡ中毒、ＡＴＮ的重要参考指标；对鉴别急性排斥反应和感染具一定的参考价值     

血小板活化状态与移植肾功能恢复关系的研究

目的 探讨外周血中血小板活化标志物—血小板表面糖蛋白Ⅲa(CD61)、溶酶体酶糖蛋白(CD63)和抗纤维蛋白原受体单抗(PAC-1)的变化与移植肾功能恢复的关系。方法 回顾性分析移植肾功能恢复正常的患者、发生急性排斥反应的患者和发生急性肾小管坏死的患者术前CD61、CD63和PAC-1的不同;前瞻性分析发生急性排斥反应的患者使用抗凝剂后,血液中CD61,CD63和PAC-1的变化、移植肾功能恢复正常的时间和1年人／肾存活率。结果 发生急性排斥反应的患者组术前外周血中的CD61、CD63和PAC-1高于发生急性肾小管坏死患者组和移植肾功能恢复正常的患者组;发生急性排斥反应的患者使用抗凝剂后血液中CD61、CD63和PAC-1下降、移植肾功能恢复正常的时间短,1年人／肾存活率高。结论 术前CD61、CD63和PAC-1较高的患者术后出现急性排斥反应的可能性大;出现急性排斥反应后,使用抗凝剂有利于移植肾功能恢复,提高1年人／肾存活率。     

大鼠同种异体动脉移植中CD4和CD8淋巴细胞数比值的变化及意义

目的 研究大鼠同种异体动脉移植术前后T淋巴细胞亚群CD4淋巴细胞计数和CD8淋巴细胞计数比值的变化及与急性免疫排斥反应的关系。方法 将45只SD雄性成年大白鼠建立同种异体动脉移植模型,按手术先后随机分为对照组(20只):取未经任何处理新鲜同种异体股动脉作移植。实验组(25只):用经深低温冷冻保存的同种异体股动脉作移植。应用免疫荧光染色技术及流式细胞仪检测2组大鼠术前和术后3、7、14、20d共5个时间组的CD4、CD8阳性细胞百分率,并计算其比值。结果 实验组术后CD4/CD8较术前无明显变化,血管通畅率为100％,未见免疫排斥反应。对照组术后CD4/CD8比值比术前显著增高(P<0.01),20 d时间组的血管通畅率为45％。术后第3天CD4/CD8比值与急性免疫排斥反应程度呈正相关。结论 深低温冷冻保存的大鼠同种异体动脉移植后CD4/CD8比值的变化和术前无明显变化,可作为术后急性免疫排斥反应的免疫学监测指标。     

1200次移植肾穿刺的并发症及临床意义分析

目的　分析移植肾穿刺术的临床意义及并发症 ,以促进移植肾活检术在肾移植患者中的广泛应用。方法　 1 994年 1月至 2 0 0 1年 1月行肾移植术的 590例患者 ,术后常规行移植肾活检术 ,肾功能短期内急剧恶化者急诊行肾穿刺活检术。采用斜角进针负压吸引法 ,对其并发症及肾活检组织病理学改变进行了分析。结果　 590例患者共行 1 2 0 0次肾穿刺术 ,穿刺成功率为 99.8% ,组织质量较好的占 81 .3 % ,光镜标本平均每份包含肾小球 (1 9.0± 9.0 )个。肾穿刺后肉眼血尿的发生率为1 .6 % ,肾周血肿的发生率为 0 .3 % ,经对症处理后缓解。出现出血并发症的患者肾组织病理学检查均有异常改变 ,包括急性肾小管坏死 (ATN) ,急性排斥反应 ,慢性排斥反应等。病情稳定患者的血清肌酐水平在肾活检后无明显的变化 .肾功能正常患者的肾活检组织病理检查发现异常的有 2 7.8% ,其中临界改变占 1 1 .9% ,动脉内膜炎占 4 .0 % ,急性排斥占 1 .4 % ,此外尚有少量的慢性排斥及间质非特异性细胞浸润。肾功能异常的患者中有 34 .9%肾组织病理表现为正常移植肾改变 ,30 .2 %的患者诊断为急性排斥 ,1 7.4 %患者诊断为临界改变 ,动脉内膜炎及ATN各占有 0 .3 %。结论　斜角进针负压吸引肾活检术在肾脏移植患者中应用成功率高 ,且较为安     

移植肾组织中C4d沉积、浆细胞聚集性浸润及其与体液性排斥反应的关系

目的 检测因排斥反应而丧失功能的移植肾组织中浆细胞的浸润情况及补体CA裂解产物C4d的沉积情况,分析浆细胞浸润、C4d沉积与体液性排斥反应的相关性.方法 切取40例因排斥反应而丧失功能的移植肾,取其组织,进行HE染色和免疫组织化学染色,依据Banff 97标准对排斥反应进行病理分型,检测肾组织中C4d、CD38和CD138的表达,分析三者之间的相关性.同时以10例非排斥因素导致移植肾功能丧失者为对照.结果 40例排斥反应中,超急性排斥反应5例,急性排斥反应9例,慢性排斥反应26例;40例中,C4d阳性17例(42.5%),CD38阳性25例(62.5%),CD138阳性23例(57.5%);有9例(22.5%)的C4d、CD38和CD138同时阳性,其中超急性排斥反应1例,急性排斥反应3例,慢性排斥反应5例.经Spearman等级相关分析,C4d的沉积与CD38和CD138的表达存在相关性(P＜0.05,P＜0.01).10例对照者中,C4d和CD38染色阳性各1例,无C4d、CD38和CD138均阳性的病例.结论 CD38和CD138与C4d的沉积存在相关性,提示移植肾中聚集性浸润的浆细胞可能通过局部分泌抗体的方式参与移植肾的体液排斥机制.     

Serial evaluation of cell surface markers for immune activation after acute renal allograft rejection by urine flow cytometry--correlation with clinical outcome

BACKGROUND: The use of urine flow cytometry (UFC) as a noninvasive tool for the diagnosis of acute and chronic rejection of the renal allograft has been previously reported. METHODS: We analyzed the expression of various cell surface antigens during a 30-day period after the diagnosis and treatment of 24 acute rejection (AR) episodes. UFC was performed on 59 urine specimens, from 17 patients meeting the diagnostic criteria for AR. UFC analysis was performed blinded to the clinical management utilizing the following fluorescinated monoclonal antibodies: anti-CD3, anti-CD14, anti-HLA-DR, anti-CD54, and anti-interleukin 2 receptor. Results were correlated with the patient's requirement for antilymphocytic drugs and increment in serum creatinine level (mg/dl) on day 30 after AR. RESULTS: HLA-DR was the most prevalent antigen noted during the first 2 days of AR (91.7% of the samples), followed by CD14 (50%) and CD54 (41.7%). After day 4 the degree of expression of HLA-DR-, CD14-, and CD54-positive cells correlated with the need for antilymphocytic drugs. CD54 was the best parameter with a sensitivity=100% and specificity=90.9% (P=0.001). Those patients who had permanent graft injury after treatment of the AR had persistence of CD54- and CD14-positive cells in the urine. CONCLUSION: Serial monitoring of urine sediments by UFC was predictive of the requirement for antilymphocytic therapy and irreversible graft damage.     

Flow cytometric evaluation of cytotoxic peripheral blood lymphocytes in acute renal graft rejection.

The presence of the S6F1+ epitope on the surface of CD8+ lymphocytes is believed to be uniquely representative of cytotoxic subpopulations. A preliminary study was conducted to evaluate the CD8+ S6F1+ peripheral lymphocytes by flow cytometry in patients undergoing renal allograft biopsy for allograft dysfunction. Lymphocytes, obtained at the time of biopsy, were analyzed by flow cytometry with CD8-FITC/S6F1-RD1 as the test monoclonal antibody and MsIgG-RD1/MsIgG-FITC as internal control. A 100% increase in S6F1+ cells over internal control was considered to be positive result. The results were correlated with the histopathologic findings in 14 instances of allograft dysfunction occurring 26.5 +/- 11.6 days posttransplantation. The histopathologic diagnosis was acute cellular rejection in eight cases, acute tubular necrosis in four, and cyclosporine nephrotoxicity in two. Flow cytometric detection of an increase in S6F1+ cells yielded a sensitivity of 87.5% and a specificity of 83.3% for the diagnosis of acute rejection. It would appear that the use of a monoclonal antibody to detect increases in the number of CD8+ S6F1+ peripheral lymphocytes is a valuable test for the detection of acute allograft rejection in the initial period after transplantation.     

Detection of B lymphocytes (CD20+) in renal allograft biopsy specimens

Acute allograft rejection represents an important complication after transplantation with significant impact on long-term graft survival. The involvement and relevance of B lymphocytes in this process is still not clear. The aim of this study was to quantify in renal allograft biopsy specimens the number of cells positive for CD20, a specific marker for B lymphocytes. Immunohistochemical techniques using monoclonal anti-CD20 antibody was used on paraffin sections from 38 renal allograft biopsy specimens. The biopsy specimens were classified into 3 groups, according to clinical and histological criteria: normal kidney, acute rejection, and chronic allograft nephropathy (CAN). In the normal kidney, no CD20(+) cells were detected. In contrast, in all cases of acute rejection and CAN, there were CD20(+) cells. The CD20(+) cells occurred in the infiltrate in 2 distinct patterns: scattered or nodular. In cases of acute rejection, the number of CD20(+) cells was significantly higher than in CAN cases (137.0 +/- 57.2 vs 45.4 +/- 9.8 cells/mm(2); P < 0.05). The nodular pattern was observed in 4 of 11 cases (36%) in the acute rejection group, and in 4 of 20 cases (20%) in the CAN cohort. In the acute rejection group, the presence of B-cell clusters tender to be associated with a higher level of serum creatinine (3.7 +/- 1.8 mg/dL vs 2.8 +/- 0.1 mg/dL in the scattered pattern group; not significant [ns]). In conclusion, these preliminary results demonstrated B lymphocytes in cases of renal allograft dysfunction, which were more pronounced in acute allograft rejection. Further analyses are required to determine whether the detection of CD20(+) cells in renal allograft biopsy specimens can be used as a prognostic marker.     

CD69 expression on peripheral CD8 T cells correlates with acute rejection in renal transplant recipients

BACKGROUND: The development of a noninvasive method to diagnose renal allograft rejection could prevent the complications associated with graft biopsy and allow more accurate surveillance of allograft function. The present study determines whether expression of CD69 on peripheral T lymphocytes of renal allograft recipients correlates with the presence of acute graft rejection. METHODS: Peripheral blood T lymphocytes from healthy volunteers, renal allograft recipients with elevated creatinine but no evidence of rejection on biopsy, and renal allograft recipients with biopsy-proven rejection were analyzed by flow cytometry for the expression of CD69 and various intracellular cytokines (interleukin-2, interferon-gamma). Results were then compared with the degree of rejection on biopsy. RESULTS: CD69 expression on CD3+, CD4+, and CD8+ T-cell subsets was low in controls and transplant recipients without allograft rejection. In contrast, patients with renal allograft rejection showed significantly elevated percentages of CD69+ cells in the CD3+ (P<0.01) and CD8+ subsets (P<0.01). The fraction of CD69+ and CD8+ T cells was found to be a more clinically useful test based on receiver-operator characteristics. CD69 expression on CD4+ T cells did not correlate with rejection. Significant intracellular cytokine levels were not detected in unstimulated T cells from any of the groups; stimulation with mitogens increased expression equally among the three groups. CONCLUSIONS: We demonstrate that expression of CD69 on CD3+ and CD8+ peripheral blood T cells correlates closely with the presence of acute graft rejection in renal allograft recipients. Measurement of this surface marker may provide a rapid, noninvasive, and accurate means by which graft rejection can be identified.     

Utility of biopsy in kidney transplants with delayed graft function and acute dysfunction

Renal biopsy is currently the gold standard to assess the causes of renal allograft dysfunction. In the present study, we prospectively assessed the role of the renal allograft biopsy in the diagnosis and treatment of renal allograft dysfunction. Seven hundred and fifteen biopsies were performed in 399 patients. The anatomopathological results in group 1 (delayed graft function) were: 60.4% acute tubular necrosis, 17.6% acute rejection, 4.3% calcineurin inhibitor toxicity, and 17.7% other diagnoses; in group 2 (acute graft dysfunction): 42.3% acute rejection, 22% acute tubular necrosis, 8.4% calcineurin inhibitor toxicity, and 27.3% other diagnoses. Among patients with delayed graft function, 42.2% of biopsies led to a change in the treatment. In 60.5%, the biopsy of patients with acute dysfunction led to a change in the patient management. In our series, the result of the biopsy disagreed with the clinical diagnosis in 39.6% and 57.7% of cases, respectively. These results demonstrated that renal graft biopsy remains an indispensable tool for the accurate management of kidney transplant patients.     

急性排斥反应时CD15和血小板/内皮细胞粘附分子在移植肾的表达

应用免疫组织化学ＳＰ法和计算机图象分析系统观察分析了１８例急性排斥反应时移植肾活检标本中ＣＤ１５和血小板／内皮细胞粘附分子的表达情况，以探讨其变化的意义。     

The presence of B-cell nodules does not necessarily portend a less favorable outcome to therapy in patients with acute cellular rejection of a renal allograft

The presence of B-cell nodules in kidney biopsies of patients undergoing acute renal allograft rejection has been reported to be associated with glucocorticoid resistance and a high risk of graft failure. In an attempt to corroborate this observation, biopsies of renal transplants that evidenced Banff grade I A acute rejection were examined for the presence of B- or T-cell nodules, the detection of which was correlated with the therapeutic response. Biopsies from 14 consecutive renal transplant recipients with a diagnosis of acute cellular rejection were examined for the presence of T (CD3-positive) or B (CD20-positive) cells by immunohistochemistry. All patients were biopsied because of a rise in serum creatinine. No biopsy showed evidence of acute humoral rejection. Immunofluorescence microscopy was negative for C4d deposition in peritubular capillaries. There were no neutrophils in the peritubular or glomerular capillaries. Five patients had T-cell nodules; four had B-cell nodules; three had both T- and B-cell nodules; two had no nodules. All biopsies contained CD3-positive cells in the tubules and in the interstitium. In all but one of the patients, episodes of acute rejection were treated with steroids (one received thymoglobulin). Furthermore two patients received mycophenolate mofetil and one, sirolimus. There were no significant differences among the groups in either the initial creatinine or the creatinine after therapy. The presence of B-cell nodules in renal allograft biopsies of patients experiencing acute cellular rejection did not portend a less favorable outcome.     

CD20+ lymphocytes in renal allografts are associated with poor graft survival in pediatric patients

BACKGROUND: The presence of CD20+ lymphocyte renal allograft infiltrates has been associated with steroid-resistant rejection and poor graft survival. We quantified the number of CD20+ lymphocytes in renal allograft biopsies and correlated the results with graft survival. We also determined the relationships between CD20+ lymphocytes and acute cellular rejection versus antibody-mediated rejection. METHODS: We examined 45 biopsy samples from 31 pediatric patients biopsied for suspicion of rejection from November 2001 to November 2004. Immunohistochemical staining for CD20 and C4d was performed on all biopsies; CD20+ cell density per high-power field (hpf) was determined for each core. Patient graft status was followed postbiopsy and documented for graft survival or failure using the cutoff date of December 31, 2005. RESULTS: Patients with 2-10 and 11-100 CD20+ cells/hpf had worse graft survival in Kaplan-Meier analysis with a hazard ratio 4.56 (CI 1.07-19.35) two years postbiopsy compared to those with 0-1 cells/hpf (P = 0.02). The presence of CD20+ lymphocytes was significantly associated with acute cellular rejection (P = 0.0001) and not associated with antibody-mediated rejection (P = 0.16). Receiver-operating curve analysis confirmed > or =3 cells/hpf correlating with acute cellular rejection, yielding sensitivity 90% and specificity 76%. CONCLUSIONS: This study shows a significant 4.5-fold risk of graft failure at two years postbiopsy with presence of > or =2 CD20+ cells/hpf. Moreover, > or =3 CD20+ lymphocytes were highly associated with acute cellular rejection. They may be functioning as professional antigen-presenting cells in the graft. In steroid-refractory cellular rejections, therapies that target B cells may prolong graft survival.     

Polyoma virus infection after renal transplantation. Use of immunostaining as a guide to diagnosis

BACKGROUND: Polyoma virus infection is characterized by lymphocytic interstitial infiltrate in the kidney, and it mimics acute rejection. The purpose of this study is to estimate renal allograft outcome with this infection and characterize the lymphocytic infiltrates in polyoma virus-infected renal allografts. METHODS: Patients who had polyoma virus inclusions in renal allograft biopsies were identified. Other viral inclusions were excluded by immunohistochemistry. The lymphocytic infiltrates of six cases of polyoma virus infection were compared with six cases of definite acute rejection by immunostaining for T and B cells. RESULTS: There were 10 cases of polyoma virus infections in renal transplant recipients. Immunosuppressants consisted of mycophenolate mofetil with tacrolimus in eight cases and mycophenolate mofetil with cyclosporine in two. The median time of diagnosis of polyoma virus infection after transplantation was 9.5 months, and the time to graft failure after the diagnosis was 4 months. Reduced allograft survival was seen in patients who had polyoma virus infection. Immunostaining for T and B cells revealed marked increase in the B cells (CD20) in renal allografts with polyoma virus infection of 21% (range, 5-40%) compared with 6% (range, 0-10%) in those with acute rejection (P=0.039). Reduced cytotoxic T cells (TIA-1: median, 7%; range, 2-15%) were seen in polyoma virus-infected allografts compared with 24% (range, 15-30%) in those patients who had acute rejection (P=0.0159). CONCLUSION: Irreversible graft failure is more prevalent with polyoma virus infection. Enhanced immunosuppressants with mycophenolate mofetil with tacrolimus may play a role in the development of this infection. An increase in CD20 and a decrease in cytotoxic T cells in allografts is characteristic of polyoma virus infection.     

A retrospective study of plasma cell infiltrates in explanted renal allografts

Renal transplantation is the most effective therapy in end-stage renal disease. The prognosis for transplant survival is still determined by rejection. When plasma cells predominate in the cellular infiltrate of allografts in rejection, it is called plasma cell-rich rejection, which has a poor prognosis. To study the correlation between plasma cell infiltration and humoral rejection, and to explore whether the local plasma cells were involved in renal allograft loss we analyzed 40 explanted grafts and 20 specimens removed for other diseases. All specimens were embedded, deparaffined, and stained with hematoxylin eosin (HE) for analysis by immunohistochemistry (IH). Renal allograft rejection was classified according to the Banff 1997 criteria with examinations for C4d deposition and CD138 expression. Positive C4d staining was defined by linear endothelial C4d deposition in > or =25% of cortical peritubular capillaries. The specimens designated as CD138-positive demonstrated strong and diffuse staining characteristics; trace or rare CD138-positive were classified as negative. Our results showed that among 40 renal graft specimens, 17 cases were C4d-positive, 23 cases were CD138-positive, and 13 cases were C4d and CD138 double-positive, namely, 42.5%, 57.5%, and 32.5%, respectively. Among the double-positive cases, there were 2 patients with a diagnosis of acute cellular rejection, 1 with hyperacute rejection, and 10 with chronic humoral rejection. C4d deposition and CD138-positive plasma cell infiltrate were related by a Spearman analysis (r = 0.330; P = .038). In the control group, there was only 1 case showing C4d positive activities. These observations suggested that infiltrated plasma cells in the renal allograft probably participate in humoral rejection through local secretion of antibodies.