A Correlation Between Histological Findings of the Blood Vessels in Patients With Chronic Renal Failure and Serum Uremic Toxins and Its Diagnostic Performance in the Assessment of the Cardiovascular Morbidity and Mortality
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 发起方
- 入组人数
- 100
- 试验地点
- 1
研究概览
简要总结
Patients treated by chronic renal replacement therapy are exposed to cardiovascular problems and suffer from an accelerated and sever atherosclerosis. Classical risk factors for atherosclerosis and cardiovascular diseases (CVD) do not explain the full risk of CVD in the dialysis patients. Additional risk factors are therefore likely to exist. The uremic syndrome is attributed to the progressive retention of a large number of compounds, which under normal conditions are excreted by the healthy kidneys. Uremic toxins such are parathormone (PTH), vitamin D and phosphates, cause development of renal osteodystrophy (ROD), i.e. disordered calcium and phosphate metabolism. Both conditions of hyperparathyroid and adynamic bone disease (ABD) lead to an elevated calcium x phosphate product and increased vascular calcification, which might occur in intimal and medial layer of the vessel wall. It is important to consider these processes separately, as the vascular consequences (occlusion with atheromatosis and vascular stiffening through medial calcification) are different. Moreover, the difference between uremic and non-uremic intimal plaque is not the size but its composition, with markedly increased calcium content. Hence, these observations have an important socio-economic impact because of the increased cardiovascular morbidity and mortality.
The investigators hypothesized that uremic toxins in dialysis patients influence directly and/or indirectly the development of atherosclerosis, vascular calcifications and CVD.
详细描述
Rationale: Patients treated by chronic renal replacement therapy are exposed to cardiovascular problems and suffer from an accelerated and sever atherosclerosis. Classical risk factors for atherosclerosis and cardiovascular diseases (CVD) do not explain the full risk of CVD in the dialysis patients. Additional risk factors are therefore likely to exist. The uremic syndrome is attributed to the progressive retention of a large number of compounds, which under normal conditions are excreted by the healthy kidneys. Uremic toxins such are parathormone (PTH), vitamin D and phosphates, cause development of renal osteodystrophy (ROD), i.e. disordered calcium and phosphate metabolism. Both conditions of hyperparathyroid and adynamic bone disease (ABD) lead to an elevated calcium x phosphate product and increased vascular calcification, which might occur in intimal and medial layer of the vessel wall. It is important to consider these processes separately, as the vascular consequences (occlusion with atheromatosis and vascular stiffening through medial calcification) are different. Moreover, the difference between uremic and non-uremic intimal plaque is not the size but its composition, with markedly increased calcium content. Hence, these observations have an important socio-economic impact because of the increased cardiovascular morbidity and mortality.
Hypothesis: We hypothesized that uremic toxins in dialysis patients influence directly and/or indirectly the development of atherosclerosis, vascular calcifications and CVD.
Objectives:
To asses the histology of arterial vessels in patients with end-stage renal failure and to evaluate its relationship with serum uremic toxins.
To determine the biochemical and clinical risk factors that might influence the development of vascular calcifications and their diagnostic performance in the assessment of CVD morbidity and mortality.
研究设计
- 研究类型
- Observational
- 观察模型
- Case Crossover
- 时间视角
- Prospective
入排标准
- 年龄范围
- 18 Years 至 65 Years(Adult, Older Adult)
- 性别
- All
- 接受健康志愿者
- 否
入选标准
- •Chronic renal failure patients with a need for creation of AV fistula
- •Dialysis patients with a need of reanastomosing of the AV fistula (thrombosis or insufficient blood flow)
排除标准
- •Malignant disease
- •Prior treatment with corticosteroids
