Levine Barton S, Rodríguez Mariano, Felsenfeld Arnold J
Nefrologia. 2014;34(5):658-69. doi: 10.3265/Nefrologia.pre2014.Jun.12379.
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.
甲状旁腺功能亢进在慢性肾脏病(CKD)中发生。对甲状旁腺激素(PTH)的降钙反应降低促成了甲状旁腺功能亢进的发展,推测是由于骨钙外流减少所致。CKD中对PTH降钙反应降低的促成因素包括:1)高磷血症;2)血清骨化三醇降低;3)PTH1受体下调;4)作用于羧基-PTH受体的大的、截短的氨基末端PTH片段;以及5)尿毒症毒素。此外,长期高剂量给予骨化三醇可能会独立于PTH减少骨钙的可交换池。本综述的目的是更好地理解上述因素如何影响CKD中骨的钙外流。总之,关于骨在血清钙调节中的作用仍有许多有待了解之处。