Description Module
The Description Module contains narrative descriptions of the clinical trial, including a brief summary and detailed description. These descriptions provide important information about the study's purpose, methodology, and key details in language accessible to both researchers and the general public.
Description Module path is as follows:
Study -> Protocol Section -> Description Module
Description Module
Ignite Creation Date:
2025-12-24 @ 3:23 PM
Ignite Modification Date:
2025-12-24 @ 3:23 PM
NCT ID:
NCT00764192
Brief Summary:
An impairment of nitric oxide (NO) bioavailability is associated with endothelial dysfunction and may contribute to the excessive incidence of cardiovascular complication in chronic haemodialysis (HD) patients. It is not known whether cell-free hemoglobin limits nitric oxide bioavailability during HD.
Detailed Description:
Cardiovascular complications are the major cause of death in end-stage renal disease (ESRD) patients undergoing chronic haemodialysis (HD).1 During haemodialysis (HD) the endothelium is the first organ to sense and to be impaired by mechanical and immunological stimuli.2 Adequate endothelial function and integrity reduce thromboembolic events, while endothelial dysfunction is an early key step in the development of atherosclerosis3-5, is involved in plaque progression6 and has been attributed to impaired nitric oxide (NO) bioactivity and enhanced formation of oxygen-derived free radicals.7 Given that endothelial dysfunction is at least in part reversible, the assessment of altered NO availability is of important diagnostic and prognostic significance and may deepen the understanding of cardiovascular disease in HD.8 Nitric oxide bioavailability has been shown to be limited by cell-free hemoglobin.9 The rates of NO consumption by cell-free and intraerythrocytic hemoglobin suggest that only when hemoglobin is physically compartmentalized within erythrocytes will NO produced by endothelial cells reach concentrations within smooth muscle necessary to activate guanylyl cyclase and cause vasodilation.10;11 However, the rate of NO scavenging is reduced 1,000-fold by sequestering hemoglobin within the red cell membrane.12;13 This mechanism is believed to be important in various conditions of health and disease.14-16 In ESRD intravascular hemolysis during HD has been described.17-19
Study:
NCT00764192
Study Brief:
Protocol Section:
NCT00764192