In CKD, inflammation, OS, mineral bone disease (low vitamin D, hyperphosphatemia, high fibroblast growth factor 23 (FGF23) and low Klotho) and the accumulation of NOS inhibitors all contribute to reduced NO bioavailability and endothelial dysfunction [21,93], resulting in the development and progression of CVD [92]. This evidence concerns the gene FGF23 and hyperphosphatemia.