Skeletal resistance to the calcemic action of parathyroid hormone in uremia: role of 1,25 (OH)2 D3.
Skeletal resistance to the calcemic action of parathyroid hormone in uremia: role of 1,25 (OH)2 D3.
复制标题
尿毒症中骨骼对甲状旁腺激素钙血作用的抵抗：1,25 (OH)2 D3 的作用。
DOI：
10.1038/ki.1976.60
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发表时间：
1976
影响因子：
19.6
通讯作者：
R. Friedler
中科院分区：
文献类型：
--
作者：
S. Massry;R. Stein;Jacob Garty;A. Arieff;J. Coburn;A. Norman;R. Friedler
研究了1，25(OH)2D3在甲状旁腺激素降钙性骨骼抵抗中的作用。观察甲状旁腺切除术(T-PTX)犬双侧输尿管结扎(11只)或双侧肾切除(8只)诱导尿毒症前、后1、2、3d静脉滴注2U/kg体重体重8h后血钙的变化。另有6只肾切除T-PTX犬，于肾切除当天及以后2天给予1，25(OH)2D3 0.68ug/d。在研究的每一天，三组患者的血肌酐水平没有差异。这项研究还包括评估假手术(5只狗)和给肾功能正常的狗(4只狗)注射1，25(OH)2D3对PTE的降钙性反应的影响，以及这种反应在同一动物中的重复性。结果表明：1)双侧输尿管结扎或肾切除1天后，PTE的降钙性反应明显减弱，但肾切除后这种损害更为严重；2)双侧输尿管结扎2天或3天后，PTE的降钙性反应与肾切除后1天相似；3)1，25(OH)2D3部分恢复了肾切除动物对PTE的降钙性反应，接近双侧输尿管结扎后1天的水平；4)假手术不影响PTE的降钙性反应，重复滴注PTE可引起相似的血钙变化。数据表明：(A)尿毒症患者骨骼对甲状旁腺素的降钙性抵抗至少部分是由于1，25(OH)2D3的缺乏；(B)尿毒症本身也可能导致这种现象；(C)双侧输尿管完全结扎一天后，肾脏仍可产生1，25(OH)2D3，但在输尿管梗阻两天后，这种能力受到影响。
Studies were carried out to investigate the role of 1,25(OH)2D3 in the skeletal resistance to the calcemic action of parathyroid hormone. The change in serum calcium after the intravenous infusion of 2 U of parathyroid extract (PTE)/kg body wt/hr for eight hours was evaluated in thyroparathyroidectomized (T-PTX) dogs before, and one, two and three days after, induction of uremia by bilateral ureteral ligation (11 dogs) or by bilateral nephrectomy (8 dogs). In another six nephrectomized and T-PTX dogs, 0.68 ug of 1, 25 (OH)2D3/day was given on the day of nephrectomy and for two days thereafter. Serum creatinine in each day of the study was not different among the three groups. The study also included the evaluation of the effect of sham operation (five dogs) and the administration of 1,25 (OH)2D3 to dogs with normal renal function (four dogs) on the calcemic response to PTE, as well as the reproducibility of such a response in the same animal. The results showed that 1) the calcemic response to PTE was markedly impaired after one day of bilateral ureteral ligation or nephrectomy, but the impairment was more severe after nephrectomy; 2) the calcemic response to PTE after two or three days of bilateral ureteral ligation was similar to that seen at one day after nephrectomy; 3) 1, 25 (OH)2D3 partially restored the calcemic response to PTE in the nephrectomized animals to levels similar to those seen after one day of bilateral ureteral ligation; 4) sham operation did not affect the response to PTE, and repeated infusion of PTE produced similar changes in the concentrations of serum calcium. The data indicate that (a) a deficiency of 1,25 (OH)2D3 is at least partly responsible for the skeletal resistance to the calcemic action of PTH in uremia; (b) uremia, per se, may also contribute to this phenomenon; and (c) the kidney after one day of complete bilateral ureteral ligation may still produce 1,25 (OH)2D3, but this ability is compromised after two days of ureteral obstruction.