[The pathophysiology of secondary hyperparathyroidism].

Secondary hyperparathyroidism (SHPT) is characterized by the acceleration of bone turnover due to the over-secretion of parathyroid hormone, which is accompanied with parathyroid hyperplasia. The pathogenesis includes the reduced production of calcitriol due to the elevated serum fibroblast growth factor 23 (FGF23) level to maintain phosphate (P) homeostasis, and its resultant hypocalcemia. Although the mechanism parathyroid glands sense P remains unknown, the expressions of calcium (Ca) sensing receptor and vitamin D receptor, which sense serum level of Ca and calcitriol respectively, down-regulate in chronic kidney disease. The rapture of feedback system including these, contributes to the development of SHPT.