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犬慢性实验性肾功能不全时甲状旁腺功能亢进的发病机制

On the pathogenesis of hyperparathyroidism in chronic experimental renal insufficiency in the dog.

作者信息

Slatopolsky E, Caglar S, Pennell J P, Taggart D D, Canterbury J M, Reiss E, Bricker N S

出版信息

J Clin Invest. 1971 Mar;50(3):492-9. doi: 10.1172/JCI106517.

DOI:10.1172/JCI106517
PMID:5545116
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC291955/
Abstract

Healthy adult dogs were subjected to stepwise reduction of nephron population so as to create the transition from normal renal function to advanced renal insufficiency. Studies were performed at each level of renal function. Glomerular filtration rate (GFR), renal phosphate clearance, and serum radioimmunoassayable parathyroid hormone (PTH) levels were measured. Two groups of animals were studied. In one, phosphorous intake was maintained at 1200 mg/day. As GFR declined, fractional phosphate excretion rose reciprocally, and PTH levels increased over 20-fold. In the second group, phosphorous intake was maintained at less than 100 mg/day. As GFR fell, fractional phosphate excretion changed little, and no increment in PTH levels occurred. The data suggest that the control system regulating phosphate excretion contributes importantly to the pathogenesis of secondary hyperparathyroidism in advancing renal insufficiency.

摘要

对健康成年犬进行逐步减少肾单位数量的操作,以实现从正常肾功能到晚期肾功能不全的转变。在每个肾功能水平上进行研究。测量了肾小球滤过率(GFR)、肾脏磷酸盐清除率和血清放射免疫法可测定的甲状旁腺激素(PTH)水平。研究了两组动物。一组中,磷摄入量维持在1200毫克/天。随着GFR下降,磷酸盐排泄分数呈反比上升,PTH水平增加了20多倍。在第二组中,磷摄入量维持在每天不到100毫克。随着GFR下降,磷酸盐排泄分数变化不大,PTH水平也没有升高。数据表明,调节磷酸盐排泄的控制系统在晚期肾功能不全继发性甲状旁腺功能亢进的发病机制中起重要作用。

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本文引用的文献

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IMMUNOASSAY OF BOVINE AND HUMAN PARATHYROID HORMONE.牛和人甲状旁腺激素的免疫测定
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Studies on the control of sodium excretion in experimental uremia.实验性尿毒症中钠排泄控制的研究。
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Experience with a radioimmunoassay of parathyroid hormone in human sera.人血清甲状旁腺激素放射免疫测定的经验
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