[Study on the relationship between chronic glomerulonephritis and human leukocyte antigen in Shandong province]

The purpose of this study was to observe the association between chronic glomerulonephritis (CGN) and human leukocyte antigen (HLA) on DNA level in order to identify susceptible and protective genes and to further explain the possible pathogenesis of CGN.

1073 renal transplantation patients with Han ethnicity were included in this study. All patients were recruited from three provincial Hospitals during the past ten years. The control group contained 7418 healthy Han volunteer donors from Shandong Hematopoietic Stem Cell Data Bank of China. We collected data about the polymorphism of HLA-I , II and DRB1. Gene frequency (GF), relative risk (RR) and correlation test were analyzed using statistical software. Some patients carrying the susceptible genes were followed up for 1,3 and 5 years, and compared their survival rate respectively.

The frequency of HLA-A23, A25,B15, B40, B53 and DRB1 * 18 alleles increased significantly in CGN patients than in controls, showing that they might be the suspicious susceptibility genes of CGN. After the follow-up periods, the prognosis of patients with the susceptible genes was worse than the controls. The frequency of haplotypes of A23-B44-DRB1 * 18, A25-B15-DRB1 * 07, A3-B70-DRB1 * 11, A68-B13-DRB1 * 04, A11-B10-DRB1 * 12 increased significantly in CGN patients than in controls. There were 8 lower frequencies alleles (including A20, A22, A35, A36, A38, B21, B73 and B78) in CGN patients that were not found in the control group. The frequencies of the HLA-A32, A33, B50, B58, B60, B71, DRB1 * 16 alleles decreased significantly in CGN patients than in controls, showing that they might be the protective genes of CGN.

Our data showed that there might be corresponding susceptibility and protective genes of CGN in Han population, in Shandong. There was significant association between the five common haplotype and CGN in Shandong population. However, the prognosis of the patients with the susceptibility genes was worse than the controls.