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临床试验/NCT00930423
NCT00930423已完成不适用

Complement Activation During Hemodialysis in Atypical Hemolytic Uraemic Syndrome as Underlying Kidney Disease.

University Hospital, Ghent1 个研究点 分布在 1 个国家目标入组 25 人开始时间: 2009年8月最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
入组人数
25
试验地点
1
主要终点
C3a-des-Arg measuring (as a marker of activation).

研究概览

简要总结

Atypical hemolytic uraemic syndrome is caused by defects in the regulating factors in the alternative pathway of the complement system. Triggering can cause an uncontrolled complement activation with endothelial damage and thrombotic micro-angiopathy, especially in the kidneys. This can result in endstage renal failure. Complement activation during hemodialysis has been described as a result of contact between blood and the dialysis membrane. Our hypothesis is that patients with atypical hemolytic uraemic syndrome have a stronger complement activation during hemodialysis than patients with another underlying kidney disease. This could be a reason to treat patients with endstage renal failure due to atypical hemolytic uraemic syndrome preferentially with peritoneal dialysis instead of hemodialysis.

研究设计

研究类型
Observational
观察模型
Case Control
时间视角
Prospective

入排标准

年龄范围
18 Years 至 —(Adult, Older Adult)
性别
All
接受健康志愿者

入选标准

  • cases: endstage renal failure due to atypical hemolytic uraemic syndrome treated with hemodialysis.
  • controls: endstage renal failure due to a non complement consuming nephropathy treated with hemodialysis.

排除标准

  • 未提供

结局指标

主要结局

C3a-des-Arg measuring (as a marker of activation).

时间窗: at time 0, at 15 minutes, at 60 minutes and at 180 minutes

white blood cell count

时间窗: before and after 15 minutes of hemodialysis

次要结局

未报告次要终点

研究者

申办方类型
Other
责任方
Sponsor

研究点 (1)

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