Jean Guillaume, Souberbielle Jean Claude, Chazot Charles
NephroCare Tassin Charcot, Sainte Foy les Lyon, 69110, France.
Service d'explorations fonctionnelles, Hôpital Necker-Enfants malades, AP-HP, Paris 75015, France.
Nutrients. 2017 Mar 25;9(4):328. doi: 10.3390/nu9040328.
Vitamin D deficiency (<20 ng/mL) and insufficiency (20-29 ng/mL) are common among patients with chronic kidney disease (CKD) or undergoing dialysis. In addition to nutritional and sunlight exposure deficits, factors that affect vitamin D deficiency include race, sex, age, obesity and impaired vitamin D synthesis and metabolism. Serum 1,25(OH)₂D levels also decrease progressively because of 25(OH)D deficiency, together with impaired availability of 25(OH)D by renal proximal tubular cells, high fibroblast growth factor (FGF)-23 and decreased functional renal tissue. As in the general population, this condition is associated with increased morbidity and poor outcomes. Together with the progressive decline of serum calcitriol, vitamin D deficiency leads to secondary hyperparathyroidism (SHPT) and its complications, tertiary hyperparathyroidism and hypercalcemia, which require surgical parathyroidectomy or calcimimetics. Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease Improving Global Outcomes (KDIGO) experts have recognized that vitamin D insufficiency and deficiency should be avoided in CKD and dialysis patients by using supplementation to prevent SHPT. Many vitamin D supplementation regimens using either ergocalciferol or cholecalciferol daily, weekly or monthly have been reported. The benefit of native vitamin D supplementation remains debatable because observational studies suggest that vitamin D receptor activator (VDRA) use is associated with better outcomes and it is more efficient for decreasing the serum parathormone (PTH) levels. Vitamin D has pleiotropic effects on the immune, cardiovascular and neurological systems and on antineoplastic activity. Extra-renal organs possess the enzymatic capacity to convert 25(OH)D to 1,25(OH)₂D. Despite many unanswered questions, much data support vitamin D use in renal patients. This article emphasizes the role of native vitamin D replacement during all-phases of CKD together with VDRA when SHPT persists.
维生素D缺乏(<20 ng/mL)和不足(20 - 29 ng/mL)在慢性肾脏病(CKD)患者或接受透析的患者中很常见。除了营养和阳光照射不足外,影响维生素D缺乏的因素还包括种族、性别、年龄、肥胖以及维生素D合成和代谢受损。由于25(OH)D缺乏,血清1,25(OH)₂D水平也会逐渐下降,同时肾近端小管细胞对25(OH)D的摄取受损、成纤维细胞生长因子(FGF)-23水平升高以及功能性肾组织减少。与普通人群一样,这种情况与发病率增加和不良预后相关。随着血清骨化三醇的逐渐下降,维生素D缺乏会导致继发性甲状旁腺功能亢进(SHPT)及其并发症、三发性甲状旁腺功能亢进和高钙血症,这些情况需要进行甲状旁腺切除术或使用拟钙剂。肾脏病预后质量倡议(KDOQI)和改善全球肾脏病预后组织(KDIGO)的专家已经认识到,CKD和透析患者应通过补充维生素D来预防SHPT,以避免维生素D不足和缺乏。已经报道了许多使用麦角钙化醇或胆钙化醇每日、每周或每月进行维生素D补充的方案。天然维生素D补充的益处仍存在争议,因为观察性研究表明,使用维生素D受体激动剂(VDRA)与更好的预后相关,并且在降低血清甲状旁腺激素(PTH)水平方面更有效。维生素D对免疫、心血管和神经系统以及抗肿瘤活性具有多效性作用。肾外器官具有将25(OH)D转化为1,25(OH)₂D的酶促能力。尽管有许多未解决的问题,但大量数据支持在肾病患者中使用维生素D。本文强调在CKD各阶段以及SHPT持续存在时联合使用VDRA进行天然维生素D替代的作用。