Several theories have been proposed in the literature, alluding to its possible association with systemic hyperphosphatemia in patients receiving chronic haemodialysis and patients with potential underlying familial traits that lead to mutation of genes involved in phosphate metabolism, e.g.FGF-23 (Fibroblast Growth Factor - 23) and GALNT-3 (Polypeptide N-Acetylgalactosaminyltransferase - 3), with presence of associated mechanical injury [3, 4, 6, 10, 13–17]. This evidence concerns the gene FGF23 and hyperphosphatemia.