Gene polymorphism in IgA nephropathy

Abstract

SUMMARY: IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. Since its original description in 1968, a large body of clinical, epidemiological and immunological studies of its pathogenesis has emerged. However, the basic molecular mechanisms of abnormal mesangial IgA deposition have remained obscure. In recent years, much clinical and experimental evidence has indicated the presence of genetic factors in the development and progression of IgAN. The search for susceptibility loci has centred on the major histocompatibility complex (MHC) using disease association in family and population studies. In addition, genes outside the realm of the MHC have been reported. The evidence for genetic factors in the onset and progression of IgAN is reviewed in this paper. The major loci influencing disease susceptibility include HLA‐DR4, ‐DQw7 and ‐DQβ, C4 null and T‐cell receptor Cα genes, whereas those affecting the natural course of IgAN include HLA‐DQβ, angiotensin‐converting enzyme D/D, T‐cell receptor Cβ and endothelial cell nitric oxide synthase 4a alleles.

IgA nephropathy recurs early in the graft when assessed by protocol biopsy

“…Several reports linked specific types of HLA to IgAN, such as HLA-DR4, HLA-DQw4 and HLA-Bw35 and HLA-B8, DR3 [16][17][18]. This suggests that various HLAassociated genes might predispose to IgAN or be related to the disease progression [19].…”