Department of Nephrology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
Nephrol Dial Transplant. 2022 May 25;37(6):1049-1058. doi: 10.1093/ndt/gfac026.
Vascular calcification is a key process involved in cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). Magnesium supplementation may counteract vascular calcification. In this study we aimed to determine whether increased dietary magnesium intake inhibits vascular calcification in CKD in vivo and explore the mechanisms underlying these effects.
Sprague Dawley rats were partially nephrectomized and fed a diet with high phosphate and either high or normal magnesium content for 16 weeks. The primary outcome was the tissue calcium content of the aorta in the high versus normal dietary magnesium group. In addition, we analysed plasma mineral concentrations, aortic vascular calcification identified with von Kossa staining, calcium apposition time and aortic expression of genes related to vascular calcification.
The number of animals in the highest tissue calcium content tertile was significantly lower in the abdominal aorta [1 (10%) versus 6 (55%); P = .03] in the high versus normal dietary magnesium group, but did not differ in the aortic arch and thoracic aorta. Von Kossa staining and calcium apposition time corresponded to these results. The median tissue calcium content was not significantly different between the groups. Serum phosphate concentrations and expression of osteogenic markers in the aorta did not differ between the groups.
This study demonstrates that increased dietary magnesium inhibits abdominal vascular calcification in an experimental animal model of CKD in vivo. These are promising results for CKD patients and further study is needed to identify the mechanisms involved and to determine the clinical relevance in patients.
血管钙化是慢性肾脏病（CKD）患者心血管发病率和死亡率的关键过程。镁补充可能对抗血管钙化。在这项研究中，我们旨在确定增加膳食镁摄入量是否能抑制 CKD 体内的血管钙化，并探讨这些影响的潜在机制。
SD 大鼠部分肾切除，给予高磷和高或正常镁含量的饮食 16 周。主要结果是高与正常饮食镁组主动脉组织钙含量。此外，我们分析了血浆矿物质浓度、von Kossa 染色鉴定的主动脉血管钙化、钙沉积时间和与血管钙化相关的主动脉基因表达。
在高镁与正常镁饮食组中，主动脉组织钙含量最高三分位的动物数量在腹主动脉中明显减少[1（10%）与 6（55%）；P=0.03]，但在主动脉弓和胸主动脉中没有差异。von Kossa 染色和钙沉积时间与这些结果相对应。两组间的组织钙含量中位数无显著差异。两组间血清磷酸盐浓度和主动脉成骨标志物的表达无差异。
本研究表明，增加膳食镁可抑制 CKD 动物模型体内腹主动脉血管钙化。这些结果对 CKD 患者有希望，需要进一步研究以确定所涉及的机制，并确定在患者中的临床相关性。
