A common and early complication of CKD is secondary hyperparathyroidism (SHPT), characterised by elevated serum parathyroid hormone (PTH) and parathyroid hyperplasia, that develops as a consequence of the mineral metabolism disturbances of several biochemical parameters (including increases in fibroblast growth factor-23 [FGF-23], and reductions in 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D], and hypocalcaemia and hyperphosphataemia) [6–9]. This evidence concerns the gene PTH and secondary hyperparathyroidism.