Angiotensin II (Ang II) overexpression promotes vasoconstriction, increased tubular sodium reabsorption, hypertension, and renal inflammation, characterized by interstitial macrophage/lymphocyte infiltration and cellular proliferation followed by an increase on extracellular matrix (ECM) deposition, loss of histological architecture, glomerulosclerosis, and interstitial fibrosis, which culminates in chronic renal insufficiency [14, 15]. This evidence concerns the gene AGT and chronic kidney disease.