摘要
高磷血症是慢性肾脏病(CKD)尤其是晚期血液透析患者常见的并发症,而高磷与动脉粥样硬化性心血管疾病(ASCVD)的发生发展密切相关。高磷血症可抑制内皮型一氧化氮合酶(eNOS)活性,导致内皮功能障碍;激活炎症小体,释放促炎因子,加剧血管炎症;扰乱胆固醇稳态,促进泡沫细胞形成。降磷治疗是改善CKD患者心血管预后的重要手段,非含钙磷结合剂在降低血磷的同时,部分研究表明,还可显著减少心血管事件和全因死亡率。本文综述了高磷血症促进动脉粥样硬化的机制,降磷药物的研究现状及减少CKD患者动脉粥样硬化发生率的机制,为维持性血液透析高磷血症患者心血管疾病防治提供理论依据。
Hyperphosphatemia is a common complication in patients with chronic kidney disease (CKD), especially those undergoing hemodialysis in advanced stages. It is closely associated with the occurrence and progression of atherosclerotic cardiovascular disease (ASCVD). Hyperphosphatemia can inhibit the activity of endothelial nitric oxide synthase (eNOS), leading to endothelial dysfunction;activate inflammasomes, release pro-inflammatory factors, and exacerbate vascular inflammation;disrupt cholesterol homeostasis and promote foam cell formation. Phosphorus-lowering therapy is an important approach to improve the cardiovascular prognosis of CKD patients. Non-calcium-based phosphate binders not only reduce serum phosphorus levels but also significantly decrease cardiovascular events and all-cause mortality. This article reviews the mechanisms by which hyperphosphatemia promotes atherosclerosis, the current research status of phosphorus-lowering drugs, and the mechanisms underlying the reduction of atherosclerosis incidence in CKD patients, providing a theoretical basis for the prevention and treatment of cardiovascular diseases in maintenance hemodialysis patients with hyperphosphatemia.
出处
《临床个性化医学》
2026年第1期546-552,共7页
Journal of Clinical Personalized Medicine
