甲状旁腺激素在肾衰竭非经典效应中的研究进展

Research Progress of Parathyroid Hormone in Non-Classical Effects of Renal Failure

甲状旁腺激素(PTH)在慢性肾脏病矿物质和骨骼代谢紊乱发病机制中起核心作用。当患者出现肾衰竭时,PTH若不能发挥其磷酸化作用,可导致高磷酸血症以及成纤维细胞生长因子23水平升高。对于肾衰竭患者,PTH的主要靶器官是骨骼,但PTH水平升高也可能通过骨骼和非骨骼机制影响患者病死率,因此降低PTH水平可提高患者生存率,且PTH水平越低越好。继发性甲状旁腺功能亢进与患者病死率之间的联系可部分解释为PTH诱导的脂肪组织褐变的作用。未来深入研究PTH在肾衰竭非经典效应中的作用机制,可以为疾病的治疗提供新思路。

Parathyroid hormone(PTH)plays a core role in the pathogenesis of chronic kidney disease-mineral and bone metabolic disorder.When patients experience renal failure,if PTH cannot exert their phosphorylation effects,it can lead to hyperphosphatemia,and elevated levels of fibroblast growth factor 23.For patients with renal failure,the main target organ of PTH is the skeleton.However,elevated PTH may also be associated with mortality through both skeleton and non-skeletal mechanisms.Therefore,reducing PTH can improve the patient survival rate,and the lower the PTH level,the better.Recent data suggests that the association between secondary hyperparathyroidism and mortality can be partially explained by the effect of PTH induced adipose tissue browning.In the future,in-depth research on the mechanism of PTH in non-classical effects of renal failure can provide new ideas for the treatment of the disease.