The pathophysiology of endothelial dysfunction in CKD includes an inflammatory response, oxidative stress, accumulation of advanced glycation end products, positive phosphorus balance with subsequent increase in fibroblast growth factor 23 and deficient active vitamin D, and an increase in certain uremic toxin levels, including asymmetric dimethylarginine and symmetric dimethylarginine, both inhibitors of endothelial NO synthase, which thus limit the availability of NO [35,36,37]. This evidence concerns the gene FGF23 and endothelial dysfunction.