Determination of HLA Tissue Type According to the Etiology of Patients with Chronic Renal Failure

根据慢性肾功能衰竭患者的病因确定HLA组织类型

阅读:1

Abstract

OBJECTIVE: Chronic kidney disease (CKD) is a prominent public health concern, is defined as functional and structural damage to the kidneys. This study aims to investigate the association between human leukocyte antigen (HLA) alleles individuals with CKD and the different etiological subgroups of diesease. METHODS: Genomic DNA was obtained from peripheral blood samples of 1,079 patients with retrospective CKD and 1,111 healthy control individuals. HLA genotyping was conducted using the Luminex based low-resolution method. Allele frequency distributions were calculated with the help of Arlequin v3.11 population genetics statistics program and SPSS v23.0 program, and p<0.05 values were accepted as significant by chi-square tests. RESULTS: HLA A*02 (21.83%), B*35 (18.30%), DRB1*11 (21.41%) alleles were observed most frequently in individuals with CKD, respectively. In our study, B*08, B*49, B*50 alleles in the HLA B locus (p=0.002, p=0.012 p=0.009) and DRB1*03, *04 alleles in the HLA DRB1 locus (p<0.001, p<0.001) were found positively associated with CKD. A*02, A*11, A*74 alleles at the HLA A locus (p=0.003, p<0.001, p=0.009) and B*27, B*39, B* alleles at the HLA B locus 40, B*59 (p<0.001, p<0.001, p<0.001, p=0.009), DRB1*07, *08, *09, *13, *16 (p<0.001, p=0.012, p=0.007, p<0.001, p<0.001) alleles were determined as negatively associated with the disease. Among the etiological groups of CKD, cystic kidney disease (36.8%), hypertension (16.8%) and urological anomalies (16.6%) were negatively associated with the HLA-DR*13 allele. CONCLUSIONS: Since CKD shows serious morbidity and mortality, this comprehensive study of HLA subgroups gave an explanatory idea about which alleles associated with the disease in terms of susceptibility and protection.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。