On the other hand, i-PTH, which is increased in the secondary hyperparathyroidism of renal disease, plays a crucial role in calcium homeostasis, and it may be a mediator of pathological calcification by both actions, preventing calcification in a dose-dependent manner by inhibiting alkaline phosphatase activity and promoting osteoblastic gene expression in bone [26,27]. This evidence concerns the gene PTH and secondary hyperparathyroidism.