原位肝移植早期肝功能不良危险因素80例分析

目的分析原位肝移植后导致移植肝初期肝功能不良(initial poor graft function,IPGF)的各种临床因素。方法回顾性分析上海交通大学医学院附属瑞金医院器官移植中心2002年6月至2004年12月80例原位肝移植的病例资料。肝移植术后72h内血清谷氨酸转氨酶(ALT)和(或)天冬氨酸转氨酶(AST)≥1500IU/L作为IPGF组,<1500IU/L作为非IPGF组。受体术前分析指标为:年龄、性别、原发疾病、Child-Pugh分级。围手术期分析指标为:心脏停搏时间(NHBT)、冷缺血时间(CIT)、供肝复温缺血时间(RWIT)、冷保存末期肝活检和术后72h内ALT和AST值。通过Logistic回归模型筛选出有可能引发IPGF的危险因素。结果NHBT、CIT、RWITIPGF组显著高于非IPGF组(P<0·05);Logistic回归模型显示NHBT是引发IPGF的危险因素(P<0·05),CIT、RWIT是可能的潜在危险因素。IPGF组中1例中度大泡脂肪变性供肝移植后出现PGNF。结论NHBT延长是引起IPGF的主要危险因素,供肝脂肪变性、CIT、RWIT延长可能是潜在危险因素。     

原位肝移植后初期肝功能不良危险因素分析

目的分析原位肝移植后导致初期肝功能不良(IPGF)发生的危险因素.资料与方法分析36次原位肝移植.肝移植术后72 h内ALT和(或)AST>1500 IU/L作为IPGF组,<1500 IU/L作为非IPGF组.受体肝移植前分析指标为年龄、原发疾病、Child分级;供肝分析指标为热缺血时间、冷保存时间、冷保存末期肝活检;手术分析指标为受体手术时间、无肝期时间.结果供肝热缺血时间IPGF组显著高于非IPGF组(P=0.04),IPGF组受体肝功能Child C者、供肝冷保存时间均高于非IPGF组,但未达到显著性差异,其余因素两组无差异(P>0.05).结论供肝热缺血时间是引起IPGF的危险因素,肝移植前肝功能Child C级、供肝冷保存时间可能是潜在危险因素.     

供肝不同程度的缺血再灌注损伤对大鼠肝移植后急性排斥反应的影响

目的 探讨大鼠供肝不同程度的缺血再灌注损伤(IRI)对肝移植后急性排斥反应(AR)的影响.方法 用随机数字表法将大鼠分为6组,每组供、受者各12只,同系移植组供肝热冷缺血时间分别为0～2和80 min,同种移植1～4组供肝热冷缺血时间分别为0～2和80 min、0～2 min和10 h、15和80 min及15 min和10 h,假手术组仅开腹游离肝脏后关腹,不行肝移植.肝移植采用改良的Kamada二袖套法.术后1、3、5、7 d,分别处死每组3只受者,取移植肝组织,行病理学检杏观察病理改变和IRI程度,按照Banff系统分级标准对AR进行评分,采用免疫组织化学法和实时聚合酶链反应法检测移植肝组织Fas、穿孔素及颗粒酶B的蛋白和mRNA表达,采用原位末端标记法检测移植肝细胞的凋亡情况.结果 假手术组、同系移植组及同种移植1～4组移植肝组织病理学改变及IRI损伤程度依次加重.术后1、3、5、7 d,假手术组、同系移植组及同种移植4组未发现AR,同种移植1～3组AR明显;随着术后时间延长,同种移植1～3组AR评分均逐渐升高,各组内不同时间点的差异均有统计学意义(P<0.05);术后相同时间点,同种移植1～3组AR评分依次升高,组间差异均有统计学意义(P<0.05).术后各时间点,假手术组、同系移植组移植肝组织中Fas、穿孔素和颗粒酶B的蛋白及mRNA均无表达,F组仅有少量表达,同种移植1～3组较其他组的表达明显升高(P<0.05);术后相同时间点,同种移植1～3组的表达量依次升高,两两比较,差异均有统计学意义(P<0.05).结论 肝移植后AR的程度与一定程度内的IRI呈正相关,但如IRI造成移植肝严重损伤,则AR的发生明显降低,Fas/FasL和穿孔素/颗粒酶B细胞凋亡途径在其中发挥重要作用.     

胰岛素门静脉灌注促进活体肝移植术后肝再生的临床研究

目的 探讨成人活体肝移植(LDLT)术后胰岛素门静脉灌注对移植肝再生的促进作用.方法 2005年7月至2007年9月间接受右肝LDLT并自愿接受术后门静脉胰岛素灌注、有完整临床资料并存活超过30 d的15例成人受者作为研究对象(胰岛素组),同期未接受门静脉胰岛素灌注治疗、有完整临床资料并存活超过30 d的连续15例成人受者作为对照组研究对象(对照组).胰岛素组受者LDLT术中从胃网膜右静脉插入一根18 G硅胶管至门静脉系统,另一端固定于腹壁,术后以2 U/h速度静脉微泵持续均匀门静脉灌注胰岛素7 d.对照组无门静脉插管及胰岛素灌注.LDLT术前1d、术后7 d及30 d检测肝功能与外周血胰岛素水平,术中、术后7 d及术后30 d测量移植肝体积(GV).以GV比例(术后移植肝体积/术中移植肝体积之百分比)和供肝受者体重比(GRWB)比例(术后GRWR/术中GRWR之百分比例)作为移植肝再生检测指标.结果 LDLT术后7d胰岛素组与对照组受者移植肝GV比例分别为(186.1±35.4)%和(160.6±22.1)%,胰岛素组移植肝再生率高于对照组(P<0.05);胰岛素组与对照组受者GRWR比例分别为(179.0±35.8)%和(156.6±18.5)%,胰岛素组移植肝再生率亦高于对照组(P<0.05).LDLT术后30 d胰岛素组与对照组受者移植肝再生率的差异无统计学意义(P>0.05).LDLT术后7 d胰岛素组患者血清总胆红素、丙氨酸转氨酶和天冬氨酸转氨酶水平低于对照组.术后两组患者外周血胰岛素水平及外周胰岛素用量的差异均无统计学意义.结论 LDLT术后胰岛素门静脉灌注可能促进术后第1周移植肝再生.     

肝脏缺血再灌注损伤分子机制的研究进展

缺血再灌注损伤(IRI)是肝移植术中不可避免的病理生理变化,是引起肝损伤的一个重要原因,可能导致肝功能衰竭,影响肝移植受者术后的近、远期疗效。参与肝脏缺血再灌注的分子进程复杂多样,所涉及的机制在很大程度上尚未阐明,并不断有新的复杂机制更新。本综述旨在总结一些重要的分子机制在肝脏IRI中的研究进展,同时概述减轻IRI的新兴策略,为临床提高肝移植疗效及移植肝生存率,提供理论和科学依据。     

依达拉奉减轻大鼠小体积肝移植物缺血再灌注损伤

目的 探讨依达拉奉减轻大鼠小体积肝移植物缺血再灌注损伤的作用及其可能机制.方法 采用成年雄性SD大鼠作为肝移植的供、受者,随机将受者分为依达拉奉组和对照组,每组8只.依达拉奉组受者移植前30 min经阴茎背静脉注射依达拉奉3 mg/kg,对照组受者仅给予等量生理盐水.采用改良的二袖套法建立大鼠40%(供肝重量与受者全肝重量比)小体积供肝肝移植模型.术后6 h时,处死两组受者,使用全自动生化分析仪检测血清天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平,采用酶联免疫吸附试验(ELISA)法检测移植肝组织中肿瘤坏死因子α(TNF-α)含量,使用相应的检测试剂盒检测移植肝组织中MDA含量以及SOD和MPO的活性.同时,取移植肝组织进行病理学检测,观察肝组织病理损伤情况.结果 术后6h,依达拉奉组受者血清AST和ALT水平分别为(825.50±72.87)U/L和(687.40±72.21)U/L,对照组分别为(1188.03±124.04)U/L和(988.66±91.07)U/L,依达拉奉组明显低于对照组,两组间比较,差异均有统计学意义(P<0.01).与对照组比较,依达拉奉组受者移植肝组织中MDA和TNF-α含量明显下降,MPO活性也明显下降,而SOD活性则明显增加,两组间比较,差异均有统计学意义(P<0.01).移植肝组织病理学检查发现,对照组肝细胞发生明显的空泡样变性伴局部坏死灶,肝小叶结构破坏,门脉周围水肿、充血,炎症细胞浸润明显;依达拉奉组肝损伤明显减轻,小叶结构保存完整,肝细胞变性、坏死轻微,炎症细胞浸润明显减少.结论 依达拉奉能够明显减轻大鼠小体积肝移植物缺血再灌注损伤,其机制可能与增强抗氧化能力、抑制脂质过氧化以及减轻炎症反应密切相关.     

大鼠供肝缺血预处理对肝移植后急性排斥反应的影响研究

目的探讨肝移植时缺血预处理(IP)对不同程度缺血再灌注损伤(IRI)后急性排斥反应(AR)的影响及机制。方法将大鼠分为6个实验组,每组供、受者各12只。同系移植组(2组)供肝热缺血时间分别为0～2 min,同种移植组(4组)供肝热缺血时间分别为0～2,15,0～2,15 min,各组冷缺血时间均为80 min;另设假手术组仅在开腹并游离肝脏后关腹。同种移植3,4组先采用入肝血流阻断法进行供肝热缺血预处理5 min。肝移植采用改良Kamada二袖套法。术后1,3,5,7 d每组分别处死3只受者,取移植肝组织,行病理学检查及观察IRI程度,用Banff系统分级标准进行AR评分,用免疫组化法和PCR法检测移植肝组织Fas,穿孔素及颗粒酶B的蛋白和mRNA表达,用TUNEL法检测移植肝细胞的凋亡率。结果同种移植1～4组移植肝病理改变及IRI程度依次加重。术后1,3,5,7 d,假手术组、同系移植组未发现AR,同种移植1～4组AR明显;同种移植3组AR评分较同种移植1组,同种移植4组较同种移植2组随术后时间延长而降低(P0.05)。术后各时点,假手术组、同系移植组移植肝中穿孔素和颗粒酶B mRNA均无表达,Fas mRNA仅有低表达;同种移植1～3组较假手术组、同系移植组、同种移植4组的表达明显升高(P0.05);术后相同时点,同种移植3组表达量较同种移植1组,同种移植4组表达量较同种移植2组下降(P0.05)。结论 IP能相应减轻肝移植相同冷、热缺血时间所致IRI程度及AR的程度,其机制是抑制细胞凋亡调控基因Fas及穿孔素/颗粒酶BmRNA和蛋白的表达。     

用于再灌注损伤研究的两种肝移植模型的筛选

目的:筛选一种用于研究肝移植过程中缺血再灌注损伤的大鼠肝移植模型.方法:将SD大鼠随机分为假手术组(S组)、原位肝移植组(OLT组)与自体肝移植组(AT组).比较各组大鼠手术时间、存活率及术后24 h血清中总胆红素(TB)、谷丙转氨酶(ALT)、谷草转氨酶(AST)及血清肿瘤坏死因子-α(TNF-α)含量,观察肝组织形态学改变.结果:与S组相比OLT组、AT组术后血清TB、ALT、AST升高明显,AT组较OLT组术后存活率明显提高,血清TB、ALT、AST及TNF-α含量明显降低,肝形态异常变化减轻(P<0.05).结论:自体肝移植模型手术简单、成功率高、可比性强,且排除了免疫损伤的影响,更好地反映了肝脏缺血再灌注损伤的病理生理过程,比较适宜作为肝移植缺血再灌注损伤研究的动物模型.     

供肝冷缺血时间延长诱发大鼠原位肝移植术后早期急性排斥反应的研究

目的 研究供肝冷缺血时间延长对大鼠原位肝移植术后早期急性排斥反应的影响.方法 选取30只健康纯系清洁级BN大鼠和30只Lewis大鼠.分别作为纯系移植和同种异体移植的供者,受者均为健康纯系清洁级BN大鼠60只,建立纯系和同种异体原位肝移植模型.根据纯系移植和同种异体移植供肝冷缺血时间的不同,将供、受者分为A、B、C和D组,每组15对.A组:供肝冷缺血1 h后进行纯系移植;B组:供肝冷缺血18 h后进行纯系移植;C组:供肝冷缺血1 h后进行同种异体移植;D组:供肝冷缺血18 h后进行同种异体移植.术后观察受者的2周存活率、移植肝组织病理学及肝功能的改变,检测受者主要组织相容性复合物(MHC)-Ⅱ类分子和核转录因子κB(NF-κB)的表达水平.结果 肝移植术后2周,A、B、C和D组的存活率分别为83.3%、66.7%、16.7%和0%,不管是纯系移植组还是同种异体移植组中供肝的冷保存时间越短,受者的存活率越高,且经肝功能检查发现冷保存时间短的受者移植肝功能恢复较好,移植肝组织病理学损伤和急性排斥反应也明显较轻.B组受者术后移植肝大量表达MHC-Ⅱ类分子,明显高于A组(P＜0.05);两同种异体移植组MHC-Ⅱ类分子的表达量较两纯系移植组增加明显,D组增加最多.A组几乎不表达NF-κB,而B组NF-κB的表达显著增加(P＜0.05);两同种异体移植组受者NF-κB的表达峰值提前.结论 冷缺血时间的延长可以诱导发生和加重大鼠原位肝移植术后早期急性排斥反应,降低术后2周存活率.     

肝移植围术期凝血功能异常的辨识与管控

肝移植是终末期肝病的最有效治疗手段.在肝移植围术期,移植受者需承受肝功能衰竭、外科创伤、移植物缺血/再灌注损伤(ischemia/reperfusion injury,IRI)及移植肝功能恢复等一系列强烈、特有的病理生理变化过程.其中,凝血功能异常的监测及管理是成功实施肝移植的关键任务与围术期管理的核心内容.及时、准确...     

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??Objective??To establish the clinic risk factors resulting in initial poor graft function (IPGF) after orthotopic liver transplantation (OLT). Methods??Eighty cases of orthotopic liver transplantation admitted between June 2002 and December 2004 in Ruijin Hospital of Shanghai Jiao Tong University were analyzed retrospectively.The group of IPGF was confirmed if alanineaminotransferase (ALT) and/or aspartate aminotransferase (AST) was above 1500 IU/L within 72 hours after OLT while non IPGF group below 1500 IU/L.Recipient associated factors before OLT analyzed were age,sex,primary liver diseases and Child??Pugh’s classification.Factors analyzed with peri??operative period were non??heart bearting time (NHBT),cold preservation time (CIT),warm ischemic time (RWIT),liver biopsy at the end of cold ischemia and ALT and/or AST within 72 hours after OLT.Logistic regression model was applied to filter the possible factors resulting in IPGF. Results??Donor NHBT,CIT and RWIT were longer significantly in IPGF group than non IPGF group (P<0.05).In logistic regression model,NHBT was the risk factor leading to IPGF (P<0.05) while CIT,RWIT were the possible risk factors.In one case of IPGF group PGNF was appeared with moderate hepatic steatosis. Conclusion??NHBT is an important risk factor leading to IPGF while steatosis in donor liver. CIT and RWIT are potential risk factors.     

Ischemia-reperfusion injury and its relationship with early allograft dysfunction in liver transplant patients

Ischemia-reperfusion injury (IRI) is believed to contribute to graft dysfunction after liver transplantation (LT). However, studies on IRI and the impact of early allograft dysfunction (EAD) in IRI grafts are limited. Histological IRI was graded in 506 grafts from patients who had undergone LT and classified based on IRI severity (no, minimal, mild, moderate, and severe). Of the 506 grafts, 87.4% had IRI (no: 12.6%, minimal: 38.1%, mild: 35.4%, moderate: 13.0%, and severe: 0.8%). IRI severity correlated with the incidence of EAD and graft survival at 6 months. Longer cold/warm ischemia time, recipient/donor hypertension, and having a male donor were identified as independent risk factors for moderate to severe IRI. Among 70 grafts with moderate to severe IRI, 42.9% of grafts developed EAD, and grafts with EAD had significantly inferior survival compared to grafts without EAD. Longer cold ischemia time and large droplet macrovesicular steatosis (≥20%) were identified as independent risk factors for EAD. Our study demonstrated that increased IRI severity was correlated with inferior short-term graft outcomes. Careful consideration of IRI risk factors during donor-recipient matching may assist in optimizing graft utilization and LT outcomes. Furthermore, identification of risk factors of IRI-associated EAD may guide patient management and possible timely graft replacement.     

Thymoglobulin induction protects liver allografts from ischemia/reperfusion injury

BACKGROUND: Interventions that minimize hepatic ischemia/reperfusion injury (IRI) can expand the donor organ pool. Thymoglobulin (TG) induction therapy has been shown to ameliorate delayed graft function and possibly decrease IRI in cadaver renal transplants recipients. This controlled randomized trial was designated to assess the ability of TG to protect against IRI in liver transplant recipients. PATIENTS AND METHODS: Twenty-two cadaveric liver transplant recipients were randomized to receive either TG (1.5 mg/kg/dose) during the anhepatic period and QOD x2 doses or no TG. No differences in recipients' demographics were present and donor characteristics were similar in terms of age, cause of death, and cold ischemia time. Maintenance immunosupression consisted of Tacrolimus (or Cyclosporine) and steroids for both groups. Donor biopsies were obtained during organ procurement, cold storage and 1 h after re-vascularization. Post-operative liver function tests were monitored. Early graft function, length of stay, patient and graft survival rates, incidence of primary non-function and rate of rejection were assessed. RESULTS: Patient and graft survival at 3 months was 100%. There was no incidence of primary graft non-function and no need for re-transplantation. The incidence of acute rejection was similar between the two groups. Patients in the TG group had significant decreases in alanine aminotransferase test at day 1 compared to the control group (p = 0.02). There were also near significant decreases of total bilirubin at day 5 and shorter length of hospitalization. Liver biopsy (at procurement, when cold, and post-reperfusion) of TG group demonstrated a trend for increased central ballooning. CONCLUSION: The TG allowed for more compromised liver grafts to be transplanted with less clinical evidence of IRI and improved function. Further studies on the degree of apoptosis in the liver biopsy post-reperfusion are underway.     

Glasgow Coma Score and Tumor Necrosis Factor α as Predictive Criteria for Initial Poor Graft Function

Initial poor graft function (IPGF) is a major factor influencing the clinical outcome after liver transplantation (LT), but there is no reliable method to assess and predict graft dysfunction. To help clinicians determine prognosis in the early postoperative period, individual parameters and complex scoring systems have been suggested, but most of them are inaccurate because of the multifactorial nature of transplantation courses. Therefore, the aim of our study was to retrospectively evaluate predictive criteria for retransplantation. Forty-two patients were enrolled in this study: 18 who experienced primary non-function (PNF) and 24 with delayed graft function (DGF). All of the patients were treated with the Molecular Adsorbent Recirculating System (MARS). They were into 3 subgroups: patients who survived without LT (n = 20; 47.7%); patients who underwent LT (n = 16; 37%), and patients who died before transplantation (n = 6; 14%). Stepwise multivariable logistic regression analysis was performed with the intent to find the risk factors for LT or death after MARS treatment (second analysis). Receiver operating characteristic (ROC) curves were performed on significant variables in the logistic regression model with the intent to individually predict variables for LT or death. After a stepwise multivariable logistic regression analysis enrolling all of the previously reported features only 2 variables, tumor necrosis factor (TFN)-α and Glasgow coma score (GCS) score, were statistically significant. TNF-α was an unique independent risk factor for retransplantation or death after MARS treatment (odds ratio [OR] 1.235; P = .013). Conversely, GCS score was protective against retransplantation or death (OR 0.150; P = .003). Starting from these assumptions, a predictive model was created using these 2 variables. On ROC analysis, the combined score showed an area under the curve greater than that of the 2 variables considered separately. Validating these results with a larger number of patients, we considered these 2 factors as subjective parameters to determine outcomes and the difference between PNF and DGF.     

Use of hepatitis C virus-positive grafts in liver transplantation: a single-centre experience

AIM: Our goal was to evaluate the outcome of HCV(+) recipients after liver transplantation (LT) using HCV(+) donors and the interaction between donor and recipient viral strain. METHODS: We performed a retrospective analysis of 21 LT performed between 1998 and 2004 using livers from HCV(+) donors in HCV(+) recipients. Two hundred thirty-seven patients with HCV cirrhosis who underwent LT with livers from HCV(-) donors were the control group. Ishak score (IS) was evaluated for all HCV(+) grafts. The considered variables included donor age, hepatic enzymes, intensive care unit stay, HCV genotype, ischemia time, recipient age, UNOS status, Child score, HCV genotype (before and 6 months after LT) and IS (after LT). We analyzed patient, graft, and disease-free survival. RESULTS: HCV(+) donors were significantly older than HCV(-) donors. The cumulative 5-year patient and graft survivals and disease free intervals were not different between groups. IS grading was more than 2/18 in two cases; the only graft with a staging score over 2/6 was retransplanted for early nonfunction. In two cases, different HCV genotypes were matched and donor strain took over the recipient strain. In one patient, donor genotyping 2a-2c took over recipient genotyping 1b and 9 months after LT recurrent hepatitis was documented, but antiviral therapy cleared HCV. CONCLUSIONS: Livers from HCV(+) donors can safely be used in HCV(+) recipients. Hepatic biopsy must always be performed; livers with bridging fibrosis should not be used. The takeover of one strain by another may change the prognosis of the patient if the predominant strain is more sensitive to antiviral therapy.     

High preoperative recipient plasma 7beta-hydroxycholesterol is associated with initial poor graft function after liver transplantation.

Oxidative stress is implicated in the pathogenesis of hepatic ischemia-reperfusion injury, a major determinant of initial poor graft function (IPGF) after orthotopic liver transplantation (OLT). We prospectively investigated the association between the recipient plasma preoperative oxidative stress and the occurrence of IPGF after deceased-donor OLT and indirectly studied the source-hepatic or extra-hepatic-of systemic oxidative stress in vivo in cirrhosis. We used a recently developed specific and sensitive mass spectrometry assay to measure 7beta-hydroxycholesterol and 7-ketocholesterol (oxysterols), markers of oxidative stress, in biological matrices. At univariate analysis, preoperative recipient 7beta-hydroxycholesterol plasma concentration was significantly higher in transplants with subsequent IPGF (n = 9) compared with those with initial good graft function (IGGF; n = 23) [mean +/- SD: 30.63 +/- 26.42 and 11.57 +/- 15.76 ng/mL, respectively] (P = 0.017). In a logistic regression model, which included also the Model for End-Stage Liver Disease (MELD) score, 7beta-hydroxycholesterol plasma concentration was an independent predictor of IPGF with an odds ratio of 1.17 (95% CI, 1.02-1.33, P = 0.028). Patients with cirrhosis (n = 32) had increased oxysterol plasma levels compared with healthy controls (n = 49); livers with cirrhosis (n = 21), however, had oxysterol content comparable with normal livers obtained from organ donors (n = 19). Oxysterols persisted elevated in plasma 1 month after OLT (n = 23). In conclusion, cirrhosis presents upregulated systemic oxidative stress likely of extrahepatic source that is associated with graft failure after OLT.     

Preconditioning of donors with interleukin-10 reduces hepatic ischemia-reperfusion injury after liver transplantation in pigs

BACKGROUND: Graft ischemia-reperfusion injury (IRI) resulting from postreperfusion inflammatory reaction remains a major cause of complications after liver transplantation. In this article, the authors investigated the effect of anti-inflammatory cytokine interleukin (IL)-10 on IRI, in a preclinical model of liver transplantation in pigs. METHODS: Donor pigs received IL-10 or saline at the start of liver graft harvesting. After 5 hr of cold ischemia, liver grafts were transplanted into untreated recipient pigs. IRI severity was measured in recipients by transaminase release and by cellular infiltration and necrosis on liver biopsy specimens. RESULTS: Donor IL-10 administration attenuated IRI, as indicated by significant reduction of mean peak of transaminase in recipients of grafts from IL-10-treated donors. In contrast, no significant differences in cell infiltration or amount of necrosis were observed on liver biopsy specimens between groups. CONCLUSIONS: Donor preconditioning with IL-10 may constitute an interesting pharmacologic approach to reduce IRI severity after liver transplantation.     

A 7-gene signature of the recipient predicts the progression of fibrosis after liver transplantation for hepatitis C virus infection

Fibrosis recurrence after liver transplantation (LT) for hepatitis C virus (HCV) is a universal event and strongly determines a patient's prognosis. The recipient risk factors for fibrosis recurrence are still poorly defined. Here we assess a genetic risk score as a predictor of fibrosis after LT. The cirrhosis risk score (CRS), which comprises allele variants in 7 genes (adaptor-related protein complex 3 S2, aquaporin 2, antizyme inhibitor 1, degenerative spermatocyte homolog 1 lipid desaturase, syntaxin binding protein 5-like, toll-like receptor 4, and transient receptor potential cation channel M5), was calculated for 137 patients who underwent LT for HCV infection and experienced HCV reinfection of the graft. The patients were stratified into 3 CRS categories: <0.5, 0.5 to 0.7, and >0.7. All patients underwent protocol biopsy after LT (median follow-up = 5 years), and liver fibrosis was assessed according to the Desmet and Scheuer score. The data were analyzed with univariate and multivariate analyses. The results showed that the highest CRS category was strongly associated with the presence of F2 or F3 fibrosis in protocol biopsy samples 1, 3, and 5 years after LT (P = 0.006, P = 0.001, and P = 0.02, respectively). Overall, 75.0% of the patients with a CRS > 0.7 developed at least F2 fibrosis, whereas 51.5% developed F3 fibrosis during follow-up. The predictive value of the CRS for fibrosis progression was independent of known clinical risk factors, including the age of the donor, the sex of the recipient, and the occurrence of acute rejection. A Kaplan-Meier analysis confirmed the prognostic value of the CRS with respect to the recurrence of severe liver fibrosis in HCV-infected patients after LT (log rank = 6.23, P = 0.03). In conclusion, the genetic signature of the recipient predicts the likelihood of severe liver fibrosis in the graft after HCV recurrence. The CRS might help with early clinical decision making (eg, the selection of patients for antiviral therapy after LT).