Resumo

NEGRI, A.L.. Bone-Kidney axis in the control of serum phosphorus and bone mineralization. Rev. argent. endocrinol. metab. [online]. 2007, vol.44, n.2, pp.86-93. ISSN 1851-3034.

The bone-kidney axis has been thought as a mechanism for the skeleton to communicate with the kidney to coordinate the mineralization of extracelular matrix with the renal handling of phosphate. Osteoblasts / osteocytes are well suited for coordinating systemic phosphate homeostasis and mineralization, since they express all of the implicated components of a possible bone-kidney axis, including PHEX, FGF-23, MEPE, and DMP1. In addition, autocrine effects of SIBLING proteins as MEPE and DMP1 on osteoblasts could regulate the production of ECM proteins that regulate mineralization. The kidney provides one of the effectors of the axis that regulates phosphate balance through the apical expression of NaPi-IIa and NaPi-IIc in proximal tubules. Central in this axis is FGF-23, produced by osteoblasts that has phosphaturic actions on the kidney. When FGF23, the first phosphatonin, was discovered to be of osteoblastic/osteocyte origin, the bone kidney axis was established. Proving the existence of this bone-kidney axis and defining its physiological role will require additional investigations.

Palavras-chave : Sodium phosphate cotransporters; FGF23; MEPE; DMP1; Fosfatonins; Bone mineralization.

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