The intricate interplay between cardiovascular disease (CVD) and CKD is underpinned by shared pathophysiological mechanisms, including the sustained activation of the renin–angiotensin–aldosterone system (RAAS), systemic inflammation, oxidative stress, endothelial dysfunction, mitochondrial impairment, and progressive tissue fibrosis [4,5,6]. This evidence concerns the gene REN and endothelial dysfunction.