Persistence of Vascular Calcification after Reversal of Uremia
Persistence of Vascular Calcification after Reversal of Uremia
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DOI：
10.1016/j.ajpath.2016.10.006
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发表时间：
2017-02-01
影响因子：
6
通讯作者：
O'Neill, W. Charles
中科院分区：
文献类型：
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作者：
Lomashvili, Koba A.;Manning, Kelly E.;O'Neill, W. Charles
血管钙化的可逆程度和可能的机制尚不清楚。为了解决这个问题，将尿毒症小鼠的钙化主动脉原位移植到正常小鼠体内，并将同种异体移植物的钙含量、组织学和矿物质与未移植的供体主动脉进行比较。移植后钙含量立即下降，但此后保持恒定，34 周后仍保持 68%+/- 12%。 X 射线衍射显示供体主动脉和同种异体移植物中都存在磷灰石。同种异体移植物中不存在破骨细胞，并且不表达巨噬细胞标记物CD11b、破骨细胞标记物抗酒石酸酸性磷酸酶或碳酸酐酶II。在严重钙化的主动脉中，最初的钙损失较少，并且与 Ca/P 比率从 1.49 增加到 1.63 相关，这与非磷灰石钙的损失一致。结果表明，尿毒症逆转后，由于缺乏磷灰石的主动吸收，血管钙化持续存在。无法吸收已形成的钙化可能会加剧血管钙化的严重程度，并表明治疗应以预防为目的。
The extent to which vascular calcification is reversible and the possible mechanisms are unclear. To address this, calcified aortas from uremic mice were transplanted orthotopically into normal mice, and the calcium content, histology, and minerals of the allografts were compared with the nontransplanted donor aorta. Calcium content decreased immediately after transplantation but remained constant thereafter, with 68%+/- 12% remaining after 34 weeks. X-ray diffraction showed the presence of apatite in both donor aortas and allografts. Osteoclasts were absent in the allografts and there was no expression of the macrophage marker CD11b, the osteoclast marker tartrate-resistant acid phosphatase, or carbonic anhydrase II. The initial loss of calcium was Less in heavily calcified aortas and was associated with an increase in the Ca/P ratio from 1.49 to 1.63, consistent with a Loss of nonapatitic calcium. The results indicate that vascular calcification persists after reversal of uremia, because of a lack of active resorption of apatite. This failure to resorb established calcifications may contribute to the severity of vascular calcification and suggests that therapy should be aimed at prevention.