title: [Phosphocalcic metabolism: regulation and explorations].
abstract: Calcium and phosphate play a key role in bone mineralization but have also many other physiological functions. The control of serum phosphate concentration is mandatory to avoid the occurrence of severe metabolic disorders, but is less tightly regulated than serum ionized calcium concentration, which is maintained in a very limited range thanks to parathyroid hormone (PTH) and the active vitamin D metabolite calcitriol. Any change in serum ionized calcium concentration is detected by the calcium sensing receptor (CaSR), a membranous protein located principally in the parathyroid glands and the kidney. A decrease in ionized calcium level inactivates the CaSR, thus stimulating PTH secretion. PTH in turn stimulates the release of calcium and phosphate from bone, renal calcium reabsorption and calcium and phosphate intestinal absorption by inducing renal calcitriol production. Moreover, PTH inhibits phosphate reabsorption in proximal tubular cells, thus contributing towards phosphate homeostasis. Fibroblast growth factor 23 (FGF23) is a circulating factor that decreases serum levels of inorganic phosphate by inhibiting renal phosphate reabsorption and calcitriol production and may have a great physiological role in phosphate homeostasis. Recently, vitamin D actions independent of calcium and phosphate homeostasis were discovered. Basal exploration of phosphocalcic metabolism abnormalities consists in measurement of serum calcium (ionized calcium if possible), phosphate, 25-hydroxy vitamine D and PTH and of 24 hours urinary calcium excretion as well as renal function. Hence, the understanding of physiopathological mechanisms has been improved by newly identified genetic disorders responsible for phophocalcic homeostasis disturbances.
authors.affiliation: Service de néphrologie et dialyses, hôpital Tenon, 4, rue de la Chine, 75020 Paris, France. marie.courbebaisse@tnn.aphp.fr
authors.forename: Marie
authors.initials: M
authors.lastname: Courbebaisse
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Souberbielle
mesh_terms: D001842:Bone and Bones / Q000378:metabolism; D002117:Calcitriol / Q000097:blood / Q000378:metabolism*; D002118:Calcium / Q000097:blood / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000097:blood / Q000378:metabolism*; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000628:therapy; D008659:Metabolic Diseases / Q000378:metabolism / Q000517:prevention & control*; D010280:Parathyroid Glands / Q000378:metabolism; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism*; D010710:Phosphates / Q000097:blood / Q000378:metabolism*; D044169:Receptors, Calcium-Sensing / Q000378:metabolism
chemical_list: D002120:Calcium Channel Agonists; C000717427:FGF23 protein, human; D010281:Parathyroid Hormone; D010710:Phosphates; D044169:Receptors, Calcium-Sensing; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D002117:Calcitriol; D002118:Calcium