Alterations in mineral metabolism are a hallmark of CKD, where increases in systemic phosphate levels, also called hyperphosphatemia, and the associated imbalance in the regulators of phosphate metabolism, i.e., increased serum concentrations of fibroblast growth factor (FGF) 23 and parathyroid hormone (PTH) along with decreased levels of vitamin D and klotho, are not only considered to serve as biomarkers for the severity of disease but might also contribute to tissue damage, such as pathologic cardiac remodeling and vascular calcification, and premature death [61]. This evidence concerns the gene PTH and hyperphosphatemia.