GA was also reported to stimulate TGF-β and increase oxidative stress, which could induce vasculopathy in experimental models.29 Therefore, the accumulation of GA as a result of impaired renal clearance was assumed to play an important role in the progression of vasculopathy in CKD patients via the promotion of oxidative stress, production of inflammatory cytokines, and endothelial damage.14 Here, TGFB1 is linked to chronic kidney disease.