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.

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