Among the mechanisms that have been described for LVH and the associated myocardial alterations are the so-called classical or traditional risk factors like hypertension, hyperlipidemia, and diabetes but also CKD-specific changes such as anemia, hypervolemia, increased sympathetic activity, hyperphosphatemia, oxidative stress, and altered expression of the fibroblast growth factor 23 (FGF-32) [7, 8]. This evidence concerns the gene FGF23 and hyperphosphatemia.