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甲状旁腺激素:一种尿毒症毒素。

Parathyroid Hormone: A Uremic Toxin.

机构信息

LIM 16, Nephrology Department, Hospital das Clínicas HCFMUSP, Universidade de São Paulo, São Paulo 05403-000, Brazil.

Post-Graduation, Universidade Nove de Julho (UNINOVE), São Paulo 01525-000, Brazil.

出版信息

Toxins (Basel). 2020 Mar 17;12(3):189. doi: 10.3390/toxins12030189.

Abstract

Parathyroid hormone (PTH) has an important role in the maintenance of serum calcium levels. It activates renal 1α-hydroxylase and increases the synthesis of the active form of vitamin D (1,25[OH]D). PTH promotes calcium release from the bone and enhances tubular calcium resorption through direct action on these sites. Hallmarks of secondary hyperparathyroidism associated with chronic kidney disease (CKD) include increase in serum fibroblast growth factor 23 (FGF-23), reduction in renal 1,25[OH]D production with a decline in its serum levels, decrease in intestinal calcium absorption, and, at later stages, hyperphosphatemia and high levels of PTH. In this paper, we aim to critically discuss severe CKD-related hyperparathyroidism, in which PTH, through calcium-dependent and -independent mechanisms, leads to harmful effects and manifestations of the uremic syndrome, such as bone loss, skin and soft tissue calcification, cardiomyopathy, immunodeficiency, impairment of erythropoiesis, increase of energy expenditure, and muscle weakness.

摘要

甲状旁腺激素(PTH)在维持血清钙水平方面起着重要作用。它激活肾脏 1α-羟化酶,增加维生素 D 活性形式(1,25[OH]D)的合成。PTH 通过直接作用于这些部位促进骨骼中钙的释放,并增强管状钙的重吸收。与慢性肾脏病(CKD)相关的继发性甲状旁腺功能亢进的特征包括血清成纤维细胞生长因子 23(FGF-23)增加,肾脏 1,25[OH]D 生成减少,其血清水平下降,肠道钙吸收减少,以及在后期出现高磷血症和 PTH 水平升高。在本文中,我们旨在批判性地讨论严重 CKD 相关的甲状旁腺功能亢进症,其中 PTH 通过钙依赖性和非钙依赖性机制导致尿毒症综合征的有害影响和表现,如骨丢失、皮肤和软组织钙化、心肌病、免疫缺陷、红细胞生成受损、能量消耗增加和肌肉无力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67b4/7150960/f0b2af1a8e77/toxins-12-00189-g001.jpg

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