Ojeda López Raquel, Esquivias de Motta Elvira, Carmona Andrés, García Montemayor Victoria, Berdud Isabel, Martín Malo Alejandro, Aljama García Pedro
Hospital Clínic, Barcelona, España.
Hospital Reina Sofía, Córdoba, España.
Nefrologia (Engl Ed). 2018 Jan-Feb;38(1):41-47. doi: 10.1016/j.nefro.2017.05.008. Epub 2017 Jul 1.
Patients on haemodialysis (HD) have a high prevalence of 25-OH-vitamin D (25-OH-D)deficiency. Secondary hyperparathyroidismis a common condition in these patients, which is very important to control. 25-OH-D is involved in regulating calcium homeostasis. As such, appropriate levels of this vitamin could help to control bone mineral metabolism.
To evaluate the effect 25-OH-D repletion in HD patients with 25-OH-D deficiency (<20ng/ml) on the control of secondary hyperparathyroidism and microinflammation status.
Prospective observational study in which stable patients on HD with 25-OH-D deficiency (<20ng/ml) were treated with oral calcifediol 0.266mcg/every 2 weeks for three months. Dialysis characteristics, biochemical parameters and drug doses administered were analysed before and after the correction of the deficiency.
Forty-five stable HD patients with a mean age of 74.08±12.49 years completed treatment. Twenty-seven patients (60%) achieved 25-OH-D levels above 20ng/ml (23 with levels>30ng/ml and 4 between 20-30ng/ml). Parathyroid hormone levels decreased in 32 of the 45 patients, 23 of which (51%) achieved a>30% decrease from baseline. In terms of concomitant treatment, we observed a significant reduction in the selective vitamin D receptor activator dose, but no changes in calcimimetic or phosphate binders administration. In terms of malnutrition-inflammation status, a decrease in C-reactive protein was noted, although other microinflammation parameters, such as activated monocytes (CD14+/CD16+ and CD 14++/CD16+) were unchanged. No changes were observed in the levels of FGF-23.
Correcting 25-OH-D deficiency in HD patients is associated with better secondary hyperparathyroidism control with lower doses of vitamin D analogues, as well as an improvement in inflammatory status. Our results support the recommendation to determine 25-OH-D levels and correct its deficiency in these patients.
血液透析（HD）患者中25-羟基维生素D（25-OH-D）缺乏的患病率很高。继发性甲状旁腺功能亢进是这些患者的常见病症，对其进行控制非常重要。25-OH-D参与调节钙稳态。因此，这种维生素的适当水平有助于控制骨矿物质代谢。
评估25-OH-D缺乏（<20ng/ml）的HD患者补充25-OH-D对继发性甲状旁腺功能亢进和微炎症状态控制的影响。
一项前瞻性观察性研究，对25-OH-D缺乏（<20ng/ml）的稳定HD患者每2周口服骨化二醇0.266mcg，持续三个月。在缺乏症得到纠正前后，分析透析特征、生化参数和给药剂量。
45例平均年龄为74.08±12.49岁的稳定HD患者完成了治疗。27例患者（60%）的25-OH-D水平达到20ng/ml以上（23例水平>30ng/ml，4例在20-30ng/ml之间）。45例患者中有32例甲状旁腺激素水平下降，其中23例（51%）较基线水平下降>30%。在联合治疗方面，我们观察到选择性维生素D受体激活剂剂量显著减少，但拟钙剂或磷结合剂的给药量没有变化。在营养不良-炎症状态方面，C反应蛋白有所下降，尽管其他微炎症参数，如活化单核细胞（CD14+/CD16+和CD14++/CD16+）没有变化。成纤维细胞生长因子23水平未观察到变化。
纠正HD患者的25-OH-D缺乏与使用较低剂量的维生素D类似物更好地控制继发性甲状旁腺功能亢进以及炎症状态改善有关。我们的结果支持在这些患者中测定25-OH-D水平并纠正其缺乏的建议。
