Información del artículo
El factor de crecimiento fibroblástico 23 (FGF-23) es una hormona derivada del hueso que participa en la regulación de la homeostasis del fósforo. Los niveles de FGF-23 se encuentran extremamente elevados en la enfermedad renal crónica y existe evidencia del papel de esta hormona en la patogénesis de los trastornos óseos y minerales en esta situación. Más aún, datos recientes implican al FGF-23 en la patogénesis de otras complicaciones sistémicas asociadas a las alteraciones óseo-minerales de la enfermedad renal crónica. La evidencia creciente de que las alteraciones del metabolismo mineral no se limitan a la enfermedad ósea ha acentuado el interés por la patofisiología y el tratamiento de las alteraciones del metabolismo mineral en la enfermedad renal crónica. Se ha propuesto que el aumento de FGF-23 es la respuesta inicial en los estadios precoces de la enfermedad renal crónica a la necesidad de proteger al organismo de los efectos adversos de la retención de fósforo. Estos aumentos de FGF-23 se asocian al riesgo creciente de mortalidad cardiovascular en los enfermos renales crónicos y son mediadores directos de toxicidad cardíaca. En esta revisión procuramos presentar aspectos relevantes de la fisiología del FGF-23 en la biología ósea y en la homeostasis mineral, así como en la fisiopatología de la enfermedad renal crónica y sus implicaciones clínicas.
Palabras clave:
TMO-ERC
Palabras clave:
Metabolismo óseo
Palabras clave:
FGF-23
Palabras clave:
Metabolismo óseo-mineral
Palabras clave:
Enfermedad renal crónica (ERC)
Fibroblast Growth Factor 23 (FGF-23) is a bone-derived hormone involved in the regulation of phosphate homeostasis. FGF-23 levels are extremely elevated in Chronic Kidney Disease (CKD) and there is evidence supporting the role of this hormone in the pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Furthermore, recent data associates FGF-23 with the pathogenesis of systemic complications of CKD-MBD. The increasing evidence that the consequences of abnormal mineral metabolism are not restricted to bone disease changed the approach to the pathophysiology and treatment of disturbed bone and mineral metabolism in CKD patients. FGF-23 has been proposed to be the initial adaptive response in early CKD to protect the organism from the adverse effects of phosphate retention. Increased levels of FGF-23 observed in CKD patients are associated with cardiovascular mortality risk and was shown to mediate direct, "off-target" toxicity to the heart. This report aims to review the relevant aspects of the physiology of FGF-23 in bone biology and mineral homeostasis and the role of FGF-23 in the pathophysiology of CKD-BMD and its clinical implications.
Keywords:
CKD-MBD
Keywords:
Bone metabolism
Keywords:
FGF-23
Keywords:
Mineral and bone metabolism
Keywords:
Chronic kidney disease (CKD)
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