Kamboj Kajal, Pariki Aruna, Singhal Manphool, Lal Anupam, Naik Sachin, Kumar Vivek, Yadav Ashok Kumar, Jha Vivekanand
Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Department of Radiodiagnosis and Imaging, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Front Immunol. 2025 Apr 24;16:1555304. doi: 10.3389/fimmu.2025.1555304. eCollection 2025.
Vitamin D deficiency, widely prevalent in patients with chronic kidney disease (CKD) could play a role in the pathogenesis of cardiovascular disease (CVD) by causing alterations in endothelial and immune function. We investigated the change in immune and vascular functions following vitamin D supplementation in non-diabetic subjects with stage 3-4 CKD and vitamin D deficiency.
In this single-arm study, non-diabetic CKD subjects aged 18-75 years, eGFR 15-60 ml/min/1.73m, and serum 25-hydroxyvitamin D levels <20 ng/ml were enrolled. Enrolled subjects received a directly observed oral dose of 300,000 IU cholecalciferol at baseline and 8 weeks. Outcome assessments, including immunological, vascular, endothelial, inflammatory, and biochemical parameters, were measured at baseline and 16 weeks.
In total, 62 subjects were studied. The mean age was 44 ± 12 years with 58% men. TH1 cells decreased from 17% (9%, 27%) to 11% (6%, 16%) (p=0.002) and TH2 cells increased from 9% (5%, 16%) to 16% (10%, 27%) (p=0.001) after cholecalciferol treatment. A significant increase in mRNA expression of vitamin D-responsive genes (cathelicidin, IL-10, VDR, and CYP27B1) was observed. The levels of pro-inflammatory cytokines (IFN-γ, TNF-α, IL-23, and IL-6) decreased whereas anti-inflammatory cytokines (IL-4, IL-10, and IL-13) showed an increase. Cholecalciferol treatment improved flow-mediated dilatation (FMD): 8.2% (6.2%, 12.1%) at baseline to 14.1% (10.0%, 20.1%) at 16 weeks (p<0.001).
This study confirms that cholecalciferol supplementation influenced immune function as it favored the TH2/TH1 phenotype, favorably affected the levels of inflammatory markers and mRNA expression of vitamin D responsive genes, and improved vascular function in CKD.
https://www.ctri.nic.in, identifier CTRI/2019/10/021494.
维生素D缺乏在慢性肾脏病（CKD）患者中广泛存在，可能通过引起内皮功能和免疫功能改变，在心血管疾病（CVD）发病机制中发挥作用。我们研究了维生素D补充对3 - 4期CKD且维生素D缺乏的非糖尿病受试者免疫和血管功能的影响。
在这项单臂研究中，纳入年龄在18 - 75岁、估算肾小球滤过率（eGFR）为15 - 60 ml/min/1.73m²且血清25 - 羟维生素D水平<20 ng/ml的非糖尿病CKD受试者。入选受试者在基线和第8周接受直接观察下的口服剂量300,000 IU胆钙化醇。在基线和第16周测量包括免疫、血管、内皮、炎症和生化参数在内的结局评估指标。
共研究了62名受试者。平均年龄为44±12岁，男性占58%。胆钙化醇治疗后，辅助性T细胞1（TH1）细胞从17%（9%，27%）降至11%（6%，16%）（p = 0.002），辅助性T细胞2（TH2）细胞从9%（5%，16%）增至16%（10%，27%）（p = 0.001）。观察到维生素D反应性基因（cathelicidin、白细胞介素10、维生素D受体和CYP27B1）的mRNA表达显著增加。促炎细胞因子（干扰素γ、肿瘤坏死因子α、白细胞介素23和白细胞介素6）水平降低，而抗炎细胞因子（白细胞介素4、白细胞介素10和白细胞介素13）水平升高。胆钙化醇治疗改善了血流介导的血管舒张（FMD）：从基线时的8.2%（6.2%，12.1%）提高到第16周时的14.1%（10.0%，20.1%）（p<0.001）。
本研究证实，补充胆钙化醇影响免疫功能，因为它有利于TH2/TH1表型，对炎症标志物水平和维生素D反应性基因的mRNA表达产生有利影响，并改善了CKD患者的血管功能。
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