“…Mesangial deposition of immune complexes, results in the activation and proliferation of these cells, and the subsequent secretion of pro-inflammatory cytokines, leading to tissue injury and disease development (6). It is suggested that the progression of immunoglobulin-A nephropathy is conducted through a four-hit processes, which is initiated with aberrant glycosylation of IgA1 and increase circulation of these galactose deficient IgA1 (Gd-IgA1), the subsequent generation of autoantibodies targeted against circulating Gd-IgA1, and the formation of immune complexes, some of which become deposited within the glomerulus structure and initiating tissue damage (1,2). In general, IgAN is most dominant in Asians, also observed in Caucasians, however, it is not as common in Africans (7).…”