Veterans Affairs Medical Center, Memphis, Tennessee; Department of Medicine, Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee; Department of Medicine, Division of Nephrology, University of Chicago, Chicago, Illinois; Department of Medicine, Division of Nephrology, Hashemite University, Zarqa, Jordan.
Veterans Affairs Medical Center, Memphis, Tennessee; Department of Medicine, Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee.
Am J Med Sci. 2013 Apr;345(4):314-320. doi: 10.1097/MAJ.0b013e31826af2d3.
25-Hydroxyvitamin D [25(OH)D] is a marker of nutritional status; however, chronic kidney disease (CKD) results in alterations in vitamin D metabolism, including the loss of vitamin D-binding proteins and alterations in CYP27B1 and CYP24 enzymes that metabolize 25(OH)D. This study was designed to determine the predictors of responsiveness to correction of vitamin D deficiency with oral vitamin D2 (ergocalciferol) in adults.
A retrospective study of 183 veterans with 25(OH)D level <30 ng/mL, who were treated with 50,000 IU per week of vitamin D2, was performed. Logistic regression models were developed to determine the factors predicting the response to treatment, defined as either the change in serum 25(OH)D level/1000 IU of vitamin D2 or the number of vitamin D2 doses (50,000 IU per dose) administered.
The mean age of the patients was 63 ± 12 years. About 87% were men and 51% diabetic, and 29% had an estimated glomerular filtration rate of <60 mL/min/1.73 m. The average number of vitamin D2 doses was 10.91 ± 5.95; the average increase in 25(OH)D level was 18 ± 10.80 ng/mL. 25(OH)D levels remained <30 ng/mL in 61 patients after treatment. A low estimated glomerular filtration rate and the presence of diabetes mellitus were significant independent predictors for inadequate response to vitamin D2 treatment in logistic regression models. Patients with CKD required greater amounts of vitamin D2 to achieve similar increases in 25(OH)D levels, versus non-CKD patients.
The presence of CKD and diabetes mellitus is associated with resistance to correction of 25(OH)D deficiency with vitamin D2 therapy. The underlying mechanism needs to be evaluated in prospective studies.
25-羟维生素 D [25(OH)D] 是营养状况的标志物;然而,慢性肾脏病 (CKD) 导致维生素 D 代谢改变,包括维生素 D 结合蛋白的丢失和 CYP27B1 和 CYP24 酶代谢 25(OH)D 的改变。本研究旨在确定口服维生素 D2(麦角钙化醇)纠正成人维生素 D 缺乏症的反应性的预测因素。
对 183 名 25(OH)D 水平 <30ng/mL 的退伍军人进行回顾性研究,他们每周接受 50,000IU 维生素 D2 治疗。建立逻辑回归模型以确定预测治疗反应的因素,定义为血清 25(OH)D 水平变化/1000IU 维生素 D2 或给予的维生素 D2 剂量(50,000IU/剂)数。
患者的平均年龄为 63±12 岁。约 87%为男性,51%患有糖尿病,29%估计肾小球滤过率 <60mL/min/1.73m。维生素 D2 剂量的平均数量为 10.91±5.95;25(OH)D 水平的平均升高为 18±10.80ng/mL。治疗后仍有 61 名患者 25(OH)D 水平<30ng/mL。在逻辑回归模型中,估计肾小球滤过率低和糖尿病是维生素 D2 治疗反应不足的显著独立预测因素。与非 CKD 患者相比,CKD 患者需要更多的维生素 D2 来达到相似的 25(OH)D 水平升高。
CKD 和糖尿病的存在与维生素 D2 治疗纠正 25(OH)D 缺乏症的抵抗力有关。需要在前瞻性研究中评估潜在机制。