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Phosphate overload accelerates vascular aging in uremic patients

机译:磷酸盐过多会加速尿毒症患者的血管衰老

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摘要

Vascular calcification is a very common event in atients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients are associated with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real “ossification” of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease.
机译:在受糖尿病和慢性肾脏病(CKD)影响的患者中,血管钙化是非常普遍的事件。最近,有大量文献证明CKD患者的矿物质和骨代谢异常与发病率和死亡率增加有关。血清磷酸盐和磷酸钙产品水平的升高在尿毒症患者血管矿化的发病机理中起重要作用,并且似乎与心血管疾病死亡率增加有关。在过去的十年中,结合经典的被动磷酸钙在软组织中的沉淀,已经证明无机磷酸酯可能直接通过CKD患者脉管中膜的真正“骨化”而引起骨骼外钙化。因此,对于受慢性肾脏疾病影响的患者,控制磷酸盐保留率现已成为治疗中更为关键的目标。

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