Reduced binding of [3H]1,25-dihydroxyvitamin D3 in the parathyroid glands of patients with renal failure.
Reduced binding of [3H]1,25-dihydroxyvitamin D3 in the parathyroid glands of patients with renal failure.
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DOI：
10.1056/nejm198706183162504
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发表时间：
1987-06
期刊：
影响因子：
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通讯作者：
A. Korkor
中科院分区：
文献类型：
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作者：
A. Korkor
本研究验证了1，25-二羟基维生素D3(1，25-(OH)2D3)与甲状旁腺受体结合改变可能参与慢性肾功能衰竭继发性甲状旁腺功能亢进症的发病机制的假说。测定了7例慢性肾功能衰竭患者增生性甲状旁腺与[~3H]1，25-(OH)_2D3的结合力。将这些值与6名接受肾移植的患者的甲状旁腺组织结合值和5名原发性甲状旁腺功能亢进症患者摘除的甲状旁腺腺瘤的结合值进行比较。我们发现，慢性肾功能衰竭患者的Nmax(1，25-(OH)2D3受体浓度的估计值)比移植肾患者(78+/-24fmoL/毫克蛋白)和原发性甲状旁腺功能亢进症患者(114+/-30)低(42+/-15fmoL/毫克蛋白)。Nmax与肾功能不全程度、血磷水平、甲状旁腺激素免疫反应性水平的对数呈负相关。这些观察表明，在慢性肾功能衰竭时，甲状旁腺组织与1，25-(OH)2D3的结合减少。这可能通过减轻1，25-(OH)2D对甲状旁腺激素分泌的抑制而参与继发性甲状旁腺功能亢进症的发病。慢性肾功能衰竭患者血清中1，25-(OH)2D的低水平可能会加重这种影响。
This study examined the hypothesis that altered binding of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) to parathyroid receptors might be involved in the pathogenesis of secondary hyperparathyroidism associated with chronic renal failure. The binding of [3H]1,25-(OH)2D3 to hyperplastic parathyroid glands obtained from seven patients with chronic renal failure was measured. These values were compared with those for binding to hyperplastic parathyroid tissue obtained from six patients who had received renal transplants and for binding to parathyroid adenomas removed from five patients who had primary hyperparathyroidism. We found that Nmax (an estimate of the concentration of 1,25-(OH)2D3 receptors) was reduced (42 +/- 15 fmol per milligram of protein) in patients with chronic renal failure as compared with patients with transplanted kidneys (78 +/- 24 fmol per milligram of protein) and patients with primary hyperparathyroidism (114 +/- 30). Nmax correlated inversely with the severity of renal dysfunction, the serum level of phosphorus, and the logarithm of the serum level of immunoreactive parathyroid hormone. These observations suggest that 1,25-(OH)2D3 binding by parathyroid tissue is reduced in chronic renal failure. This may contribute to the pathogenesis of secondary hyperparathyroidism by reducing the inhibition by 1,25-(OH)2D of parathyroid hormone secretion. The low serum levels of 1,25-(OH)2D in chronic renal failure may accentuate this effect.