Effect of N-acetylcysteine (NAC) on Hydrogen Sulfide (H2S) in Chronic Kidney Disease (CKD)
Status:
Completed
Trial end date:
2011-12-01
Target enrollment:
Participant gender:
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.