IgA nephropathy is one of the most common forms of glomerulopathies. It is an immune complex-mediated glomerulonephritis diagnosed by the presence of mesangial IgA deposits that are often associated with mesangial cell proliferation. The IgG, C-3, IgM, or other immunoglobulin light chains may be co-existed with IgA. Its pathogenesis suggested that it is responsible for enhancing the production of proinflammatory cytokines, chemokines, and growth factors. Platelet-derived growth factor (PDGF) has also been implicated as a modulator of disease activity. Immune thrombocytopenic purpura (ITP) is a bleeding disorder caused by thrombocytopenia that is not associated with a systemic disease. Its pathogenesis suggested an autoimmune disease in which IgG is thought to damage megakaryocytes, which are the precursors of platelet cells. Several studies reported that PDGF levels were higher in normal subjects than in patients with ITP. Moreover, ITP is a disease related to the antibody. Thus, our aim is to examine whether a similar pathophysiological relationship exist between ITP and IgAN that may be mediated by PDGF and/or IgG.