Caclium, phosphorus, and bone in renal disease and transplantation.
Caclium, phosphorus, and bone in renal disease and transplantation.
复制标题
肾脏疾病和移植中的钙、磷和骨。
DOI：
10.1001/archinte.1969.00300150061009
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发表时间：
1969
影响因子：
--
通讯作者：
L. Avioli
中科院分区：
文献类型：
--
作者：
N. Bricker;E. Slatopolsky;E. Reiss;L. Avioli
钙-磷-骨的相互关系在进展性肾病中逐渐被破坏。甲状旁腺激素（PTH）的释放，通常协调钙稳态的要求，成为主导改变磷酸盐平衡。随着肾单位破坏的每一波，据信会发生短暂的高磷酸盐血症、短暂的低钙血症和PTH水平的逐步升高。当肾小球滤过率福尔斯低于25 ~ 30 ml/min时，高磷血症持续存在，低钙血症倾向持续存在，对PTH释放的刺激被夸大。维生素D抵抗导致低钙血症（从而加速PTH分泌）和骨软化。在接受长期血液透析的患者中，如果高磷酸盐血症和低钙血症持续存在，PTH水平可能保持较高，纤维性骨炎可能进展。成功的肾移植通常会导致甲状旁腺功能亢进的消退和维生素D敏感性的恢复;然而，甲状旁腺功能亢进可能会缓慢消退，必须预防严重的高钙血症。真正的PTH自主性释放在慢性肾脏疾病中很少发生。
Calcium-phosphate-bone interrelationships become disrupted progressively in advancing renal disease. Parathyroid hormone (PTH) release, normally attuned to calcium homeostasis requirements, becomes dominated by alterations in phosphate balance. With each wave of nephron destruction, there is believed to occur transient hyperphosphatemia, transient hypocalcemia, and a step-wise rise in PTH levels. When the glomerular filtration rate falls below 25 to 30 ml per minute, hyperphosphatemia persists, hypocalcemia tends to persist, and the stimulus to PTH release is exaggerated. Vitamin D resistance contributes both to hypocalcemia (thus to accelerated PTH secretion) and to osteomalacia. In patients receiving long-term hemodialysis, if hyperphosphatemia and hypocalcemia persist, PTH levels may remain high and osteitis fibrosa may progress. Successful renal transplantation typically leads to regression of hyperparathyroidism and restoration of vitamin D sensitivity; however, hyperparathyroidism may regress slowly, and severe hypercalcemia must be guarded against. True autonomy of PTH release apparently occurs rarely in chronic renal disease.