Cha Ran-hui, Yang Seung Hee, Kim Hyo Sang, Kim Sun Moon, Park Myoung Hee, Ha Jongwon, Kim Yon Su
Department of Internal Medicine, Seoul National University College of Medicine, Korea.
Nephrol Dial Transplant. 2009 Sep;24(9):2919-25. doi: 10.1093/ndt/gfp317. Epub 2009 Jun 26.
Acute rejection (AR) contributes to the development of chronic allograft nephropathy that is the major cause of graft failure. We analyzed the 59029G>A polymorphism and an internal 32 bp deletion (CCR5 32) of CCR chemokine receptor 5 (CCR5) Delta and tried to prove the hypothesis that genetic interactions between the donor and the recipient influence the development of AR.
We detected genetic polymorphisms by the TaqMan(R) method and by sizing PCR amplicons (n = 486). The primary outcomes were early acute rejection (EAR) and repeated early acute rejection (RR). We defined EAR as the occurrence of a biopsy-proven AR within 3 months after transplantation.
The development of EAR was dependent on the number of A alleles in recipients and showed a dose-response relationship (P = 0.002). When we combined the number of A alleles in both donor and recipient, episodes of EAR and RR were more prevalent as the allelic number increased (A allelic number 0 & 1, 2 versus 3 & 4, P = 0.048; 0 & 1 versus 3 & 4, P = 0.006). Statistical significance was preserved after multivariate analysis of sex, HLA mismatch and type of donor with the recipient's age as the continuous term. Also, graft survival was different according to the presence of the A allele, i.e. recipients carrying A allele (+) grafts showed poor graft survival (P = 0.008 by a log-rank test). Again, the number of A alleles affected graft survival as the recipients who carried more A alleles had poor graft survival (A allele number 0 & 1 versus 2 versus 3 & 4, P = 0.011; 0 & 1 versus 3 & 4, P = 0.08; 0 & 1 versus 2, P = 0.002; by a log-rank test). All of the participants were wild-type homozygotes for CCR5Delta32.
The A allele of CCR5 59029G>A was a risk factor for EAR and RR. As the number of A alleles increased, episodes of EAR were more frequently observed.
急性排斥反应(AR)会导致慢性移植肾肾病的发生,而慢性移植肾肾病是移植失败的主要原因。我们分析了CC趋化因子受体5(CCR5)的59029G>A多态性和一个32bp的内部缺失(CCR5 32),并试图证明供体与受体之间的基因相互作用会影响AR发生发展的这一假设。
我们采用TaqMan方法和对PCR扩增产物进行大小测定的方法检测基因多态性(n = 486)。主要观察指标为早期急性排斥反应(EAR)和反复早期急性排斥反应(RR)。我们将EAR定义为移植后3个月内经活检证实的AR的发生。
EAR的发生取决于受体中A等位基因的数量,并呈现剂量反应关系(P = 0.002)。当我们综合考虑供体和受体中A等位基因的数量时,随着等位基因数量的增加,EAR和RR的发作更为普遍(A等位基因数量0&1、2与3&4相比,P = 0.048;0&1与3&4相比,P = 0.006)。在对性别、HLA错配以及供体类型与受体年龄作为连续变量进行多因素分析后,统计学意义依然存在。此外,根据A等位基因的存在情况,移植肾存活率也有所不同,即携带A等位基因(+)移植肾的受体移植肾存活率较差(对数秩检验,P = 0.008)。同样,A等位基因的数量影响移植肾存活率,因为携带更多A等位基因的受体移植肾存活率较差(A等位基因数量0&1与2与3&4相比,P = 0.011;0&1与3&4相比,P = 0.08;0&1与2相比,P = 0.002;对数秩检验)。所有参与者均为CCR5Delta32的野生型纯合子。
CCR5 59029G>A的A等位基因是EAR和RR的危险因素。随着A等位基因数量的增加,EAR发作更频繁被观察到。