Recent studies have shown that coreceptors Klotho and FGFR1c, which activate FGF-23, decreased in uremic parathyroid hyperplasia, and high serum FGF-23 levels could be explained by Klotho-FGFR1c complexes of secondary hyperparathyroidism [14, 15]. This evidence concerns the gene KL and secondary hyperparathyroidism.