Laboratory of Biology and Organisms Physiology, Team of Bioenergetics and Intermediary Metabolism Nutrition and Dietetics in Human Pathologies Post Graduate School, University of Sciences and Technology Houari Boumediene, El Alia, Bab Ezzouar, Algiers 16123, Algeria.
Biology and Physiology Laboratory, Ecole Nationale Supérieure de Kouba, Algiers 16308, Algeria.
Nutrients. 2022 May 29;14(11):2285. doi: 10.3390/nu14112285.
The 25-hydroxyvitamin D3 (25OHD3) deficiency in chronic kidney disease (CKD) is associated with immune system dysfunction (pro-inflammatory cytokines storm) through macrophages renal infiltration, oxidative stress (OxS) damage and athero-thromboembolic risk. Conversely, cholecalciferol supplementation (25OHD-S) prevents kidney fibrosis by inhibition of vascular calcification and nephrotic apoptosis (nephrons reduction). The objective of this study was to investigate the pleiotropic effects of 25OHD-S on immunomodulation, antioxidant status and in protecting against thromboembolic events in deficiency CKD Black and White individuals living in the Southern Sahara (SS). The oral 25OHD-S was evaluated in 60,000 IU/month/36 weeks versus in 2000 IU/day/24 weeks in Black (n = 156) and White (n = 150). Total serum vitamin D was determined by liquid chromatography-tandem mass spectrometry. All biomarkers of pro-inflammatory cytokines (PIC) were assessed by ELISA tests. OxS markers were assessed by Randox kits. Homocysteine and lipoproteine (a) were evaluated by biochemical methods as biomarkers of atherothromboembolic risk. All statistical analyses were performed with Student’s t-test and one-way ANOVA. The Pearson test was used to calculate the correlation coefficient. The means will be significantly different at a level of p value < 0.05. Multiple logistic regressions were performed using Epi-info and Statview software. Vitamin D deficiency alters the PIC profile, OxS damage and atherothrombogenic biomarkers in both SS groups in the same manner; however, these disorders are more acute in Black compared to White SS individuals. The results showed that the serum 25OHD3 concentrations became normal (>75 nmol/L or >30 ng/mL) in the two groups. We have shown that the dose and duration of 25OHD-S treatment are not similar in Black SS residents compared to White SS subjects, whilst the same inhabit the south Sahara environment. It appears that a high dose intermittent over a long period (D60: 36 weeks) was more efficient in Black people; while a lower dose for a short time is sufficient (D2: 24 weeks) in their White counterparts. The oral 25OHD-S attenuates PIC overproduction and OxS damage, but does not reduce athero-thromboembolic risk, particularly in Black SS residents.
25-羟维生素 D3（25OHD3）缺乏与慢性肾脏病（CKD）患者的免疫系统功能障碍（促炎细胞因子风暴）有关，其通过巨噬细胞肾浸润、氧化应激（OxS）损伤和动脉粥样血栓栓塞风险而发生。相反，胆钙化醇补充（25OHD-S）通过抑制血管钙化和肾病细胞凋亡（肾单位减少）来预防肾纤维化。本研究旨在探讨 25OHD-S 在免疫调节、抗氧化状态和预防居住在撒哈拉以南非洲（SS）的黑人和白人 CKD 患者血栓栓塞事件中的多种作用。通过液相色谱-串联质谱法测定口服 25OHD-S（60000IU/月/36 周）与 2000IU/天/24 周对黑人（n=156）和白人（n=150）的影响。通过 ELISA 试验评估所有促炎细胞因子（PIC）生物标志物。通过 Randox 试剂盒评估 OxS 标志物。通过生化方法评估同型半胱氨酸和脂蛋白（a）作为动脉粥样血栓栓塞风险的生物标志物。所有统计分析均采用学生 t 检验和单因素方差分析。Pearson 检验用于计算相关系数。p 值<0.05 时，均值将有显著差异。使用 Epi-info 和 Statview 软件进行多变量逻辑回归。维生素 D 缺乏以相同的方式改变了 SS 两组的 PIC 谱、OxS 损伤和动脉粥样血栓形成生物标志物；然而，与 SS 白人相比，这些紊乱在 SS 黑人中更为严重。结果表明，两组血清 25OHD3 浓度均恢复正常（>75nmol/L 或>30ng/mL）。我们已经表明，与 SS 白人相比，SS 黑人居民的 25OHD-S 治疗剂量和持续时间不同，而他们同样居住在撒哈拉以南的环境中。高剂量间歇治疗（D60：36 周）在黑人中更有效；而在白人中，低剂量短期治疗（D2：24 周）就足够了。口服 25OHD-S 可减轻 PIC 过度产生和 OxS 损伤，但不能降低动脉粥样血栓栓塞风险，尤其是在 SS 黑人居民中。
