Abstract

IgA nephropathy (IgAN) is the most common glomerulonephritis in the world. Recent researches showed that the galactose-deficient IgA1 (Gd-IgA1) laid the molecular basis of pathogenesis of IgAN. In addition, the involvement of mucosal and complement immune abnormalities in the pathogenesis of IgAN may also provide new directions for the diagnosis and treatment of IgAN. Key words: IgA nephropathy; Galactose-deficient-IgA1; Mucosal immunity; Complement system; Pathogenesis

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