FGF23 and mineral metabolism, implications in CKD-MBD.

نویسندگان

  • Mariano Rodríguez
  • Ignacio López
  • Juan Muñoz
  • Escolástico Aguilera-Tejero
  • Yolanda Almaden
چکیده

Correspondence: Mariano Rodríguez Servicio de Nefrología. Hospital Universitario Reina Sofía. REDINREN, IM IBIC, Córdoba. [email protected] The regulation of mineral metabolism is achieved trough a complex interaction of hormonal factors and target organs. Before the discovery of FGF23 we believed that the regulation of serum calcium and phosphate was mainly the result of changes in PTH and vitamin D acting on bone, kidneys and intestine. Parathyroids and kidneys were responsible for the production of PTH and 1,25(OH)2D3 respectively. Presently we know that FGF23 is produced by bone so the bone is not longer just a target organ but an active endocrine organ that participate in the regulation of mineral metabolism by sending signals through FGF23. Nephrologists are knowledgeable about the regulation of calcium and phosphate otherwise it is difficult to understand and manage the disturbances of mineral metabolism that are always present in patients with CKD. Changes in mineral metabolism in CKD are now described as chronic kidney disease-mineral and bone disorders (CKD-MBD). The pathology derived from CKD-MBD includes not only bone abnormalities but cardiovascular disease with a devastating prevalence of vascular calcification. The severity of CKD –MBD is associated with increased mortality in CKD patients.

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عنوان ژورنال:
  • Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia

دوره 32 3  شماره 

صفحات  -

تاریخ انتشار 2012