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继发性甲状旁腺功能亢进症(SHPT)是慢性肾病(CKD)患者常见严重并发症之一。随着CKD的进展,骨化三醇生成减少,成纤维细胞生长因子23(FGF-23)的表达升高,加之肾小球滤过率的下降,出现低血钙、高血磷,导致甲状旁腺激素(PTH)的合成和分泌的增加,从而导致SHPT的发生。另外钙敏感受体和维生素D受体的下调,也导致SHPT的发生发展[1]。已有研究发现,在CKD 3、4、5期分别约有40%、70%
Secondary hyperparathyroidism (SHPT) is one of the most common serious complications in patients with chronic kidney disease (CKD). With the progress of CKD, calcitriol production decreased, the expression of fibroblast growth factor 23 (FGF-23) increased, coupled with the glomerular filtration rate decreased, hypocalcemia, hyperphosphatemia, leading to thyroid Increased synthesis and secretion of parathyroid hormone (PTH), resulting in the occurrence of SHPT. In addition calcium-sensitive receptors and vitamin D receptor down, also led to the occurrence and development of SHPT [1]. It has been found that in CKD 3,4,5 were about 40%, 70%