跳至主要内容
临床试验/NCT01232257
NCT01232257已完成3 期

Effect of N-acetylcysteine on Hydrogen Sulfide in Chronic Kidney Disease

A.C. Abrahams1 个研究点 分布在 1 个国家目标入组 28 人开始时间: 2011年7月最近更新:
适应症
干预措施
相关药物

试验速览

阶段
3 期
状态
已完成
发起方
入组人数
28
试验地点
1
主要终点
Hydrogen sulfide (H2S)

研究概览

简要总结

Cardiovascular morbidity and mortality is high in CKD patients. Nitric oxide (NO) deficiency plays a crucial role in progression of CKD. This leads to endothelial dysfunction, hypertension, and inflammation. Hydrogen sulfide (H2S) could serve as a backup mechanism for NO deficiency in CKD. N-acetylcysteine (NAC) is a derivate of cysteine and this is the main substrate for H2S production. Therefore, NAC should enable us to stimulate H2S production in humans. Our objective is to investigate the effect of NAC on plasma H2S levels and on markers of oxidative stress, inflammation, and endothelial dysfunction in healthy volunteers, CKD patients, and dialysis patients. We hypothesize that there is an increase in H2S levels after treatment with NAC.

研究设计

研究类型
Interventional
分配方式
Non Randomized
干预模型
Single Group
主要目的
Treatment
盲法
None

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

  • 未提供

排除标准

  • 未提供

研究组 & 干预措施

Healthy volunteers

Experimental

干预措施: N-acetylcysteine (Drug)

CKD patients

Experimental

Patients with CKD stage 3-4 (GFR 15-60 ml/min)

干预措施: N-acetylcysteine (Drug)

Hemodialysis patients

Experimental

干预措施: N-acetylcysteine (Drug)

Peritoneal dialysis patients

Experimental

干预措施: N-acetylcysteine (Drug)

结局指标

主要结局

Hydrogen sulfide (H2S)

时间窗: After 48 hours

Investigate the effect of N-acetylcysteine on plasma H2S levels and on markers of oxidative stress, inflammation, and endothelial dysfunction in healthy volunteers, CKD patients, and dialysis patients

次要结局

未报告次要终点

研究者

发起方
A.C. Abrahams
申办方类型
Other
责任方
Sponsor Investigator
主要研究者

A.C. Abrahams

MD

UMC Utrecht

研究点 (1)

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