AGT and glomerulosclerosis: Cytokines will elevate TGF-β, and induce glomerular sclerosis and tubular interstitial fibrosis, which finally leads to DN.[16,17] In vitro experiments suggest that cytokines related to vascular injury and angiogenesis including fibrocyte growth factor, TGF-β and AngII can reduce OIF expression.[18] The activation of the AngII system is a major cause of renal hypertension supporting the finding of this research where SBP increased as OIF decreased with the deterioration of DN.