These alterations are multifactorial in nature and share a variety of risk factors including afterload related factors (hypertension and arterial stiffness), volume overload, CKD-mineral bone disorders (CKD-MBD) like hyperphosphatemia, hyperparathyroidism, reduced vitamin D receptor activation and high Fibroblast Growth Factor 23 (FGF23), sympathetic overactivity, nitric oxide (NO) inhibition by the accumulation of endogenous inhibitors of NO synthase, inflammation, and oxidative stress [11]. This evidence concerns the gene FGF23 and hyperparathyroidism.