The mechanisms of hypertension in CKD include volume overload, neuronal/hormonal alterations, salt retention, and endothelial dysfunction (Ku et al., 2019), in which angiotensin II (Ang‐II), the main player of the renin–angiotensin system (RAS), is one of the major contributors to the progression of renal fibrosis, inflammation, glomerular injury, and CKD (Haase, 2011; Mezzano et al., 2001). This evidence concerns the gene AGT and Hypertension.