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Effect of N-acetylcysteine (NAC) on Hydrogen Sulfide (H2S) in Chronic Kidney Disease (CKD)

NCT01232257 · Status: COMPLETED · Phase: PHASE3 · Type: INTERVENTIONAL · Enrollment: 28

Last updated 2012-10-26

No results posted yet for this study

Summary

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.

Conditions

Interventions

DRUG

N-acetylcysteine

4 gifts of N-acetylcysteine 600 mg BID

Sponsors & Collaborators

  • A.C. Abrahams

    lead OTHER

Principal Investigators

  • M C Verhaar, MD, PhD · UMC Utrecht

  • A C Abrahams, MD · UMC Utrecht

Study Design

Allocation
NON_RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Model
SINGLE_GROUP

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2011-07-31
Primary Completion
2011-12-31
Completion
2011-12-31

Countries

  • Netherlands

Study Locations

More Related Trials

Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT01232257 on ClinicalTrials.gov