Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries

NCT ID: NCT00764192

Last Updated: 2009-01-13

Basic Information

• Recruitment Status: COMPLETED
• Clinical Phase: NA
• Total Enrollment: 14 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2006-10-31
• Study Completion Date: 2007-10-31

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

Conditions

Hemodialysis

Study Design

• Allocation Method: NA
• Intervention Model: SINGLE_GROUP
• Primary Study Purpose: BASIC_SCIENCE
• Blinding Strategy: NONE

Study Groups

1

14 HD patients are studied before and after a single HD using a polysulphone dialyser.

Group Type: EXPERIMENTAL

blood sample

Intervention Type: PROCEDURE

blood sample before and after a single HD

Flow-mediated dilation (FMD) before and after a single HD

Intervention Type: PROCEDURE

measuring of the flow-mediated dilation using high-resolution ultrasound

Interventions

blood sample

blood sample before and after a single HD

Intervention Type: PROCEDURE

Flow-mediated dilation (FMD) before and after a single HD

measuring of the flow-mediated dilation using high-resolution ultrasound

Intervention Type: PROCEDURE

Other Intervention Names

biochemistry; endothelial function

Eligibility Criteria

Inclusion Criteria

• patients older 21 years dependent on HD for more than 6 months

Exclusion Criteria

• known HD associated hypotension intake of nitrate

• Minimum Eligible Age: 21 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Heinrich-Heine University, Duesseldorf

OTHER

Sponsor Role: collaborator

RWTH Aachen University

OTHER

Sponsor Role: lead

Responsible Party

RWTH Aachen University, Medical Clinic I, University Hospital

Principal Investigators

Christian Meyer, MD

Role: PRINCIPAL_INVESTIGATOR

RWTH Aachen University, Medical Clinic I

Locations

University Hospital

Aachen, North Rhine-Westphalia, Germany

Countries

Germany

References

Meyer C, Heiss C, Drexhage C, Kehmeier ES, Balzer J, Muhlfeld A, Merx MW, Lauer T, Kuhl H, Floege J, Kelm M, Rassaf T. Hemodialysis-induced release of hemoglobin limits nitric oxide bioavailability and impairs vascular function. J Am Coll Cardiol. 2010 Feb 2;55(5):454-9. doi: 10.1016/j.jacc.2009.07.068.

Reference Type: DERIVED

PMID: 20117459 (View on PubMed)

Other Identifiers

EK DD 2022 CM

Identifier Type: -

Identifier Source: org_study_id