Coronary calcification in hemodialysis patients

慢性肾脏疾病(CKD)患者死亡率增加， 心血管疾病(CVD)约占这些地区死亡人数的50% 病人。这是一种非典型的动脉粥样硬化，钙质沉积增加。 动脉粥样硬化斑块，增厚的中膜和不完全解释的传统 风险因素。血管钙化(VC)，导致动脉僵硬和左 心肌肥厚可能是导致心肌梗死的主要原因。近期 有证据表明慢性炎症状态和骨矿物质的改变 透析患者常见的代谢和循环VC抑制物可能起作用 在血管钙化过程中起着重要作用。我们正在回应PA-06-148 与肾脏相关的试点和可行性方案，目标是使用 确定新的、非传统危险因素的流行病学和生化方法 治疗CKD患者的CVD。冠状动脉钙化(CAC)在这种情况下很常见 并与死亡率的增加有关。脉搏波速度有 也被发现与该患者的死亡率独立相关。这两个 非侵入性测量将能够提供对 每个受试者的血管钙化和顺应性。我们假设在个体中 炎症程度最高，骨代谢改变最多，CAC 在12个月内比那些 正常的炎症状态和骨代谢。我们建议招募一个125人的队列 发生无症状透析患者并测量CAC和PWV 未雨绸缪。我们的主要分析工具将是Wilcoxon秩和检验和标准 混合效应增长曲线模型。研究结果将有助于识别风险因素。 我们可以在未来的随机临床试验中改变其风险分布。此外，它还将 洞察当前的临床治疗是否增加了 我们透析人群中的钙化。

Patients with chronic kidney disease (CKD) have an increased mortality rate and cardiovascular disease (CVD) accounts for approximately 50% of deaths in these patients. It is an atypical form of atherosclerosis with increased deposition of calcium in the atherosclerotic plaque, thickening of the media and not fully explained by traditional risk factors. Vascular calcification (VC) which leads to arterial stiffness and left ventricular hypertrophy is likely to be a major contributant to the pathology. Recent evidence suggest that a chronic inflammatory state and alterations of bone mineral metabolism and circulating VC inhibitors which are common in dialysis patients may play an important role in the vascular calcification process. We are responding to PA-06-148 Pilot and Feasibility Program Related to the Kidney whose objective is to use epidemiological and biochemical approaches to identify new, non-traditional risk factors for CVD in patients with CKD. Coronary artery calcification (CAC) is common in this population and has been associated with increased mortality. Pulse wave velocity has also been found to be independently associated with mortality in this patients. These two non-invasive measurements will be able to provide an assessment of the degree of vascular calcification and compliance in each subject. We hypothesize that in individuals with the highest levels of inflammatory and alteration of bone metabolism, CAC will be more prevalent and progress more rapidly in a 12-month period than in those with normal inflammatory state and bone metabolism. We propose to enroll a cohort of 125 incident asymptomatic dialysis patients and obtain measurements of CAC and PWV prospectively. Our main tool for analysis will be Wilcoxon rank-sum test and standard mixed effects growth curve models. The study findings will aid in identifying risk factors whose risk profile we can alter in future randomized clinical trials. In addition, it will provide insight on whether current clinical therapies are increasing the burden of calcification in our dialysis population.