慢性肾脏病继发性甲状旁腺功能亢进的发病机制研究进展

来源 :现代生物医学进展 | 被引量 : 0次 | 上传用户:lfw_1988
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继发性甲状旁腺功能亢进是慢性肾脏病的常见并发症,严重影响患者的生活质量和生存率。其发病机制主要包括低钙血症、高磷血症、活性维生素D缺乏、维生素D受体及钙敏感受体表达下调等。近年来,成纤维细胞生长因子23在继发性甲状旁腺功能亢进发病机制中的作用,也越来越受到重视。上述机制均可导致慢性肾脏病患者的甲状旁腺细胞增生,由多克隆增生逐渐发展为单克隆增生、腺瘤等,甲状旁腺功能亢进也逐渐加重。现就慢性肾脏病继发性甲状旁腺功能亢进的发病机制的进展做一综述。 Secondary hyperparathyroidism is a common complication of chronic kidney disease, seriously affecting the quality of life and survival of patients. The pathogenesis include hypocalcemia, hyperphosphatemia, active vitamin D deficiency, vitamin D receptor and calcium-sensitive receptor downregulation. In recent years, the role of fibroblast growth factor 23 in the pathogenesis of secondary hyperparathyroidism, more and more attention. These mechanisms can lead to hyperplasia of parathyroid cells in patients with chronic kidney disease, polyclonal hyperplasia gradually evolved into monoclonal hyperplasia, adenoma, etc., hyperparathyroidism also gradually increased. The pathogenesis of secondary hyperparathyroidism in chronic kidney disease is reviewed.
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