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Vol. 34. Núm. 5.Septiembre 2014
Páginas 545-692
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Vol. 34. Núm. 5.Septiembre 2014
Páginas 545-692
DOI: 10.3265/Nefrologia.pre2014.Jun.12379
Acceso a texto completo
Calcio sérico y huesos: efectos de la hormona paratiroidea, del fosfato, de la vitamina D y de la uremia
Serum calcium and bone: effect of PTH, phosphate, vitamin D and uremia
Visitas
8757
Barton S. Levinea, Mariano Rodríguezb, Arnold J. Felsenfelda
a Departments of Medicine, VA Greater Los Angeles Healthcare System and the David Geffen School of Medicine at UCLA, Los Angeles, CA, USA,
b Department of Nephrology, Red in Ren. IMIBIC. Hospital Universitario Reina Sofía, Córdoba, Spain,
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Información del artículo

El hiperparatiroidismo se desarrolla en la enfermedad renal crónica (ERC). La disminución de la respuesta calcémica a la hormona paratiroidea (PTH) contribuye al desarrollo de hiperparatiroidismo y es probable que se deba a una reducción de la emisión de calcio de los huesos. Entre los factores que contribuyen a la disminución de la respuesta calcémica a la PTH en la ERC se encuentran: 1) la hiperfosfatemia; 2) la disminución del calcitriol sérico; 3) la desensibilización del receptor PTHR1; 4) la presencia de fragmentos de gran tamaño de los extremos aminoterminales de la hormona paratiroidea que actúan en el receptor carboxi-PTH y 5) las toxinas urémicas. Asimismo, la administración prolongada de una dosis elevada de calcitriol podría disminuir la reserva intercambiable de calcio independiente de la hormona paratiroidea. El objetivo de esta revisión es facilitar la comprensión de cómo afectan los factores mencionados anteriormente a la emisión de calcio procedente del hueso en la ERC. Como conclusión, aún queda mucho por aprender acerca del papel de los huesos en la regulación del calcio sérico.

Palabras clave:
Vitamina D
Palabras clave:
Uremia
Palabras clave:
Fosfato
Palabras clave:
Hormona paratiroidea
Palabras clave:
Calcio
Palabras clave:
Hueso

Hyperparathyroidism develops in chronic kidney disease (CKD). A decreased calcemic response to parathyroid hormone (PTH) contributes to the development of hyperparathyroidism and is presumed due to reduced calcium efflux from bone. Contributing factors to the decreased calcemic response to PTH in CKD include: 1) hyperphosphatemia; 2) decreased serum calcitriol; 3) downregulation of the PTH1 receptor; 4) large, truncated amino-terminal PTH fragments acting at the carboxy-PTH receptor; and 5) uremic toxins. Also, prolonged high dose calcitriol administration may decrease the exchangeable pool of bone calcium independent of PTH. The goal of the review is to provide a better understanding of how the above cited factors affect calcium efflux from bone in CKD. In conclusion, much remains to be learned about the role of bone in the regulation of serum calcium.

Keywords:
Vitamin D
Keywords:
Uremia
Keywords:
Phosphate
Keywords:
Parathyroid hormone
Keywords:
Calcium
Keywords:
Bone
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