Chronic Kidney Disease, Chronic Kidney Failure, End Stage Kidney Disease, End Stage Renal Disease
Conditions
Keywords
Chronic kidney disease, Chronic kidney failure, End stage kidney disease, End stage renal disease, Hydrogen sulfide, N-acetylcysteine, Acetylcysteine
Brief 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.
Interventions
4 gifts of N-acetylcysteine 600 mg BID
Sponsors
Study design
Eligibility
Inclusion criteria
Healthy volunteers: * Adult (\> 18 years and older) * Healthy, as assessed by medical history, blood pressure, plasma creatinine, and urine dipstick * No medication use CKD patient: * Adult (\> 18 years and older) * CKD stage 3-4 (GFR 15-60 ml/min) Hemodialysis patient: * Adult (\> 18 years and older) * Hemodialysis patient Peritoneal dialysis patient: * Adult (\> 18 years and older) * Peritoneal dialysis patient
Exclusion criteria
* Unable to give informed consent * Hypersensitivity to N-acetylcysteine * Pregnancy
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Hydrogen sulfide (H2S) | 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 |
Countries
Netherlands