RESUMO
Although immunoglobulin A (IgA) nephropathy (IgAN) is considered as an immune-mediated inflammatory disease,the pathogenesis and mechanisms associated with its progression have not been completely understood.To date,the potential pathogenesis of IgAN is thought to be a possible increase of galactose-deficient IgA1,followed by binding to antiglycan antibodies to form immune complexes,which are deposited in the glomerular mesangium and lead to the activation of complement pathways and initiation of immune-mediated inflammation.Activation of alternative and lectin complement pathways,complement components,and complement regulatory proteins play important roles in the pathogenesis and progression of IgAN.Complement components and complement regulatory factors in the renal tissue,urine,and serum samples are considered to be useful predictive biomarkers to evaluate the activation of the complement system and determine the prognosis of IgAN.The application of novel techniques such as the genome-wide association study would promote further research to determine the role and mechanisms of action of the complement system,whereby it could be used as a new therapeutic target for the management of IgAN.