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首页> 外文期刊>Advances in renal replacement therapy >Pathogenesis of parathyroid dysfunction in end-stage renal disease.
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Pathogenesis of parathyroid dysfunction in end-stage renal disease.

机译:终末期肾脏疾病甲状旁腺功能不全的发病机制。

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摘要

The parathyroid functions to maintain normal calcium and phosphate homeostasis and is cenral to normal bone physiology. In end-stage renal disease (ESRD), there is a failure of these normal homeostatic mechanisms with the frequent development of secondary hyperparathyroidism, which contributes to the pathogenesis of renal bone disease. The phosphate retention of ESRD, together with the reduced serum calcium and 1,25-dihydroxycholecalciferol vitamin D(3) (1,25[OH](2)D(3)) concentrations are the known factors that determine the progression to secondary hyperparathyroidism. 1,25(OH)(2)D(3) markedly decreases parathyroid hormone (PTH) gene transcription, whereas the effects of calcium and phosphate are on PTH mRNA stability, PTH secretion, and parathyroid cell proliferation. The mechanisms of these effects are discussed in this review.
机译:甲状旁腺的功能是维持正常的钙和磷稳态,并以正常的骨生理为中心。在终末期肾病(ESRD)中,这些正常的体内平衡机制失败,继发性甲状旁腺功能亢进症的频繁发生,导致肾骨病的发病机理。 ESRD的磷酸盐保留,降低的血清钙和1,25-二羟基胆钙化固醇维生素D(3)(1,25 [OH](2)D(3))浓度是决定继发甲状旁腺功能亢进发展的已知因素。 1,25(OH)(2)D(3)显着降低甲状旁腺激素(PTH)基因的转录,而钙和磷酸盐对PTH mRNA稳定性,PTH分泌和甲状旁腺细胞增殖的影响。这些影响的机制在本综述中进行了讨论。

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