Phosphorus accelerates the development of parathyroid hyperplasia and secondary hyperparathyroidism in rats with renal failure
Phosphorus accelerates the development of parathyroid hyperplasia and secondary hyperparathyroidism in rats with renal failure
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DOI：
10.1016/s0272-6386(96)90473-4
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发表时间：
1996-10-01
影响因子：
13.2
通讯作者：
Slatopolsky, E
中科院分区：
文献类型：
--
作者：
Denda, M;Finch, J;Slatopolsky, E
几项研究表明，磷（P）限制，独立于血清离子钙和1，25-（OH）（2）D-3水平，可预防慢性肾功能衰竭患者和动物的甲状旁腺增生和继发性甲状旁腺功能亢进。然而，磷在这些异常发病机制中的直接作用仍有争议，因此，为了研究磷在这些异常发展中的直接作用，对雌性Sprague-Dawley大鼠进行了5/6肾切除或假手术，然后将动物分为两个饮食组（高P：0.8%P饮食，低P：0.2%P饮食），在以下时间间隔，每组每个时间点处死6至8只大鼠：0，1，2，4天，1，2，3，4周，高磷饮食尿毒症大鼠血清全段甲状旁腺激素（PTH）水平在肾切除后1天升高，在研究期间，高水平的磷持续存在，喂饲高磷饮食的尿毒症大鼠的甲状旁腺生长在尿毒症2天内明显，到2周时增加近两倍。然而，这些异常并没有发展在尿毒症大鼠喂养低磷饮食。高磷饮食的尿毒症大鼠血清磷水平显著高于低磷饮食的尿毒症大鼠，但血清离子钙和1，25-（OH）（2）D-3水平无显著差异。这些结果表明，磷加速了肾衰竭大鼠甲状旁腺增生和继发性甲状旁腺功能亢进的发展。限制磷摄入可防止这些异常，而与血清离子钙和1，25-（OH）（2）D-3的变化无关。(C)1996年由国家肾脏基金会，公司。
Several studies have suggested that phosphorus (P) restriction, independent of serum levels of ionized calcium and 1,25-(OH)(2)D-3, may prevent parathyroid hyperplasia and secondary hyperparathyroidism in patients and animals with chronic renal failure, A direct role of phosphorus in the pathogenesis of these abnormalities is, however, still controversial, Thus, studies were performed to examine the direct role of phosphorus on the development of these abnormalities, Female Sprague-Dawley rats underwent 5/6 nephrectomy or sham operation, The animals were then divided into two dietary groups (High-P: 0.8% P diet, Low-P: 0.2% P diet), Six to eight rats per group per time-point were killed at the following intervals: 0, 1, 2, and 4 days, and 1, 2, 3, and 4 weeks, Serum intact parathyroid hormone (PTH) levels in uremic rats fed the high-P diet increased 1 day after nephrectomy, and high levels persisted for the duration of the study, Parathyroid gland growth in uremic rats fed the high-P diet was apparent within 2 days of uremia and increased nearly twofold by 2 weeks. These abnormalities, however, did not develop in uremic rats fed the low-P diet. Serum P levels in uremic rats fed the high-P diet were significantly higher than those of uremic rats fed the low-P diet, but there was no significant difference in serum ionized calcium or 1,25-(OH)(2)D-3 levels, These results demonstrate that phosphorus accelerates the development of parathyroid hyperplasia and secondary hyperparathyroidism in rats with renal failure, and that phosphorus restriction prevents these abnormalities independent of changes in serum ionized calcium and 1,25-(OH)(2)D-3. (C) 1996 by the National Kidney Foundation, Inc.