Razzaque Mohammed S
Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Contrib Nephrol. 2013;180:74-85. doi: 10.1159/000346784. Epub 2013 May 3.
Vascular calcification or mineralization is a major complication seen in patients with advanced stages of chronic kidney disease (CKD), and it is associated with markedly increased morbidity and mortality. Most of the CKD-related vascular mineralization is attributable to abnormal mineral ion metabolism. Elevated serum calcium and phosphate levels, along with increased calcium-phosphorus byproduct, and the use of active vitamin D metabolites are thought to be the predisposing factors for developing vascular mineralization in patients with CKD. Recent experimental studies have shown that vascular mineralization can be suppressed by reducing serum phosphate levels, even in the presence of extremely high serum calcium and 1,25-dihydroxyvitamin D levels, indicating that reducing 'phosphate toxicity' should be the important therapeutic priority in CKD patients for minimizing the risk of developing vascular mineralization and the disease progression.
血管钙化或矿化是慢性肾脏病(CKD)晚期患者常见的主要并发症,与发病率和死亡率显著增加相关。大多数与CKD相关的血管矿化归因于矿物质离子代谢异常。血清钙和磷水平升高,以及钙磷副产物增加,加上活性维生素D代谢产物的使用,被认为是CKD患者发生血管矿化的诱发因素。最近的实验研究表明,即使在血清钙和1,25-二羟基维生素D水平极高的情况下,通过降低血清磷水平也可以抑制血管矿化,这表明降低“磷毒性”应是CKD患者降低发生血管矿化风险和疾病进展风险的重要治疗重点。