Role of vitamin D deficiency in chronic kidney disease
Role of vitamin D deficiency in chronic kidney disease
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DOI：
10.1359/jbmr.07s203
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发表时间：
2007-12-01
影响因子：
6.2
通讯作者：
Sprague, Stuart M.
中科院分区：
文献类型：
--
作者：
Gal-Moscovici, Arica;Sprague, Stuart M.
慢性肾脏病(CKD)已被认为是一个重大的公共卫生问题，目前约有2000万美国人，或类似于11%的成年人口患有CKD。与慢性肾脏病相关的发病率的一个重要来源是矿物质代谢紊乱的发展，几乎所有患者在疾病发展过程中都会发生这种情况，并与骨丢失和骨折、心血管疾病、免疫抑制和死亡率增加有关。随着肾脏疾病的发展，功能性肾脏质量减少，并有保留磷的趋势。功能性肾脏质量的减少和磷的滞留会降低肾脏的α-羟基酶活性，从而减少肾脏骨化三醇的产生。维持正常血钙和磷平衡的进一步补偿包括增加甲状旁腺素和潜在的其他磷酸因子的产生和释放，如成纤维细胞生长因子-23(FGF23)。FGF23的这种增加有助于维持正常的血磷而不依赖甲状旁腺素，但也可能通过抑制肾脏α-羟基酶的活性而加重骨化三醇缺乏症。骨化三醇的减少还会导致进一步的甲状旁腺机能亢进和甲状旁腺增生，因为骨化三醇通常会抑制甲状旁腺激素原和甲状旁腺细胞的增殖。
Chronic kidney disease (CKD) has been recognized as a significant public health problem, with similar to 20 million Americans, or similar to 11% of the adult population, currently living with CKD. A significant source of morbidity associated with CKD is the development of disturbances of mineral metabolism, which occurs in virtually all patients during the progression of their disease, and is associated with bone loss and fractures, cardiovascular disease, immune suppression, and increased mortality. As kidney disease develops, there is decreased functional renal mass and a tendency to retain phosphorus. The reduction in functional renal mass and the retained phosphorus act to reduce renal la-hydroxylase activity and thus the renal production of calcitriol. Further compensation to maintain normal serum calcium and phosphorus homeostasis includes increased production and release of PTH and potentially other phosphaturic factors, such as fibroblast growth factor-23 (FGF23). This increase in FGF23 contributes to maintain normal serum phosphate independent of PTH but may worsen calcitriol deficiency by also inhibiting renal la-hydroxylase activity. The decrease in calcitriol also results in promoting further hyperparathyroidism and parathyroid gland hyperplasia, because calcitriol normally inhibits the production of prepro-PTH and parathyroid cell proliferation.