Hypocalcemia may not be essential for the development of secondary hyperparathyroidism in chronic renal failure.
Hypocalcemia may not be essential for the development of secondary hyperparathyroidism in chronic renal failure.
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低钙血症对于慢性肾功能衰竭继发性甲状旁腺功能亢进症的发生可能不是必需的。
DOI：
10.1172/jci112666
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Slatopolsky,E
中科院分区：
文献类型：
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作者：
Lopez-Hilker,S;Galceran,T;Chan,YL;Rapp,N;Martin,KJ;Slatopolsky,E
低钙血症是慢性肾脏病继发性甲状旁腺功能亢进的主要原因。对尿毒症患者甲状旁腺细胞的研究表明，钙调节激素（甲状旁腺激素[PTH]）分泌的设定点发生了变化。在犬中进行了研究，以进一步阐明这种新的潜在机制。通过给予高钙饮食预防尿毒症犬的低钙血症。最初，离子钙为4.79 +/- 0.09 mg/dl，并逐渐增加至5.30 +/- 0.05 mg/dl。尽管离子钙中度增加，但免疫反应性PTH（iPTH）从64 +/- 7.7增加至118 +/- 21 pg/ml。血清1，25（OH）2D 3从25.4 +/- 3.8降至12.2 +/- 3.6 pg/ml。在另外两组犬中进行了进一步研究。一组接受150-200 ng，第二组接受75-100 ng的1，25（OH）2D 3，每日两次。1，25（OH）2D 3水平从32.8 +/- 3.5增加至最大值69.6 +/- 4.4 pg/ml。在第二组中，肾切除术后的血清1，25（OH）2D 3水平在研究期间保持正常。在1，25（OH）2D 3处理的两个组中，氨基末端iPTH均未增加。总之，犬在任何时候都没有发生低钙血症;然而，iPTH水平增加了84%，表明低钙血症本身可能不是继发性甲状旁腺功能亢进发生的唯一因素。
Hypocalcemia is the main factor responsible for the genesis of secondary hyperparathyroidism in chronic renal disease. Studies with parathyroid cells obtained from uremic patients indicate that there is a shift in the set point for calcium-regulated hormone (parathyroid hormone [PTH] secretion. Studies were performed in dogs to further clarify this new potential mechanism. Hypocalcemia was prevented in uremic dogs by the administration of a high calcium diet. Initially, ionized calcium was 4.79 +/- 0.09 mg/dl and gradually increased up to 5.30 +/- 0.05 mg/dl. Despite a moderate increase in ionized calcium, immunoreactive PTH (iPTH) increased from 64 +/- 7.7 to 118 +/- 21 pg/ml. Serum 1,25(OH)2D3 decreased from 25.4 +/- 3.8 to 12.2 +/- 3.6 pg/ml. Further studies were performed in two other groups of dogs. One group received 150-200 ng and the second group 75-100 ng of 1,25(OH)2D3 twice daily. The levels of 1,25(OH)2D3 increased from 32.8 +/- 3.5 to a maximum of 69.6 +/- 4.4 pg/ml. In the second group the levels of serum 1,25(OH)2D3 after nephrectomy remained normal during the study. Amino-terminal iPTH did not increase in either of the two groups treated with 1,25(OH)2D3. In summary, the dogs at no time developed hypocalcemia; however, there was an 84% increase in iPTH levels, suggesting that hypocalcemia, per se, may not be the only factor responsible for the genesis of secondary hyperparathyroidism.