Patel Tejas V, Singh Ajay K
Renal Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Semin Nephrol. 2009 Mar;29(2):113-21. doi: 10.1016/j.semnephrol.2009.01.004.
Decline in renal function is related directly to cardiovascular mortality. However, traditional risk factors do not fully account for the high mortality in these patients. Activated vitamin D, a hormone produced by the proximal convoluted tubule of the kidney, appears to have beneficial effects beyond suppressing parathyroid hormone (PTH). However, activated vitamin D also can cause hypercalcemia and hyperphosphatemia in chronic kidney disease. Newer agents such as vitamin D receptor activators (eg, paricalcitol) suppress PTH with reduced risk of hypercalcemia and hyperphosphatemia. Recent evidence from animal and preliminary human studies supports an association between vitamin D receptor activators and reduced risk of cardiovascular disease deaths, irrespective of PTH levels. New pathways of vitamin D regulation also have been discovered, involving fibroblast growth factor-23 and klotho. Although considerable work has been performed to advance our understanding of the effects of vitamin D in health and chronic kidney disease, more investigations and randomized trials need to be performed to elucidate the mechanistic underpinnings of these effects.
肾功能下降与心血管死亡率直接相关。然而，传统危险因素并不能完全解释这些患者的高死亡率。活性维生素D是由肾近端曲小管产生的一种激素，似乎除了抑制甲状旁腺激素（PTH）外还有有益作用。然而，活性维生素D在慢性肾脏病中也可导致高钙血症和高磷血症。新型药物如维生素D受体激活剂（如帕立骨化醇）在降低高钙血症和高磷血症风险的同时抑制PTH。动物和初步人体研究的最新证据支持维生素D受体激活剂与降低心血管疾病死亡风险之间存在关联，而与PTH水平无关。维生素D调节的新途径也已被发现，涉及成纤维细胞生长因子-23和klotho。尽管已经开展了大量工作来增进我们对维生素D在健康和慢性肾脏病中作用的理解，但仍需要进行更多研究和随机试验来阐明这些作用的机制基础。
