目的探讨HLA-A、B、DRB1高分辨等位基因表达与因IgA肾病(IgAN)最终导致慢性肾功能衰竭(CRF)的相关性。方法采用聚合酶链反应一直接测序分型技术(PCR-SBT)对来自于广东省3所三级甲等医院共191例因IgAN所致CRF患者(研究组)和503例健康献血者(对照组)进行HLA—A、B、DRB1高分辨等位基因分型,比较两组等位基因的频率,分析因IgAN所致CRF与HLA基因多态性的关系。结果(1)研究组中共表达出HLA等位基因A位点25个,B位点48个,DRB1位点32个。(2)与对照组比较,研究组HLA-A*2901(Pc=0.033,OR=10.738,95%CI为1.193~96.691),HLA-DRB*1106(Pc=0.0001,OR=0.969,95%CI为0.944-0.994),HLA-DRB1*1202(Pc=0.002,OR=1.859,95%CI为1.259~2.745),HLA-DRB1*1401(Pc=0.021,OR=0.984,95%CI为0.967-0.998),HLA-DRB1*1602(Pc=0.015,OR=1.915,95%CI为1.157-3.17)基因频率较对照组显著升高,差异均有统计学意义。结论HLA-A*2901及HLA-DRB1*1106、*1202、*1401和*1602高分辨等位基因与IgAN所致CRF呈易感关联,由此推测HLA基因多态性表达与IgAN所致CRF的发生可能有密切的遗传免疫关联性。
Objective To investigate the correlation between human leukocyte antigens-A, -B, - DRB1 (HLA-A, -B, -DRB1 ) high-resolution alleles and chronic renal failure (CRF) caused by immunoglobulin-a nephropathy (IgAN). Method The polymerase chain reaction-sequence-based typing (PCR-SBT) method was used to investigate the genotypes of HLA-A, -B and -DRB1 high- resolution alleles in 191 cases of CRF caused by IgAN (experimental group) and 503 healthy blood donors (control group). The alleles frequencies between two groups were compared and the association between CRF caused by IgAN and the polymorphism of HLA was analyzed. Result (1) There were 25 alleles at A locus, 48 alleles at B locus and 32 alleles at DRB, locus in experimental group. (2)The genetic frequency of HLA-A * 2901 [Pc= 0.033, OR= 10. 738, 95% CI (1. 193, 96. 691)], HLA-DRB1 * 1106 [Pc= 0. 0001, OR= 0. 969, 95% CI (0. 944, 0. 994)], HLA-DRB1 * 1202[Pc = 0. 002, OR = 1. 859, 95% CI (1. 259, 2. 745)], HLA-DRB1 * 1401 [Pc = 0. 021, OR = 0.984, 95% CI (0.967,0.998)], HLA-DRB1 * 1602[Pc= 0.015, OR= 1.915, 95% CI (1. 157, 3. 17)] in experimental group was higher than in control group (P〈0. 05). Conclusion There is susceptibility association of HLA-A * 2901, HLA-DRB1 * 1106, HLA-DRB1 * 1202, HLA-DRB1 * 1401, HLA-DRB, * 1602 with CRF caused by IgAN. It is concluded that there is a close genetic and immunological correlation between HLA alleles and the pathogenesis of CRF caused by IgAN.