Although the exact mechanisms of nephropathy are not fully understood, AGEs, oxidative stress, and the activation of the renin-angiotensin-aldosterone system (RAAS) facilitate and strengthen these changes partially through activation of TGF-β1 signaling and increased vascular endothelial growth factor (VEGF) expression in the kidney toward progression of fibrosis and renal failure [70–72]. This evidence concerns the gene VEGFA and Renal insufficiency.