Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries

Hemodialysis Clinical Trial

Official title:

Angiologic Study of the Influence of Hemodialysis on Endothelial Function

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00764192
• Other study ID #: EK DD 2022 CM
• Status: Completed
• Phase: N/A
• First received: September 26, 2008
• Last updated: January 12, 2009
• Start date: October 2006
• Est. completion date: October 2007

Study information

• Verified date: January 2009
• Source: RWTH Aachen University
• Contact: n/a
• Is FDA regulated: No
• Health authority: Germany: Ethics Commission
• Study type: Interventional

Clinical Trial 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.

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

Recruitment information / eligibility

• Status: Completed
• Enrollment: 14
• Est. completion date: October 2007
• Est. primary completion date: February 2007
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 21 Years and older

Eligibility

Inclusion Criteria:

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

Exclusion Criteria:

• known HD associated hypotension intake of nitrate

Study Design

Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science

Related Conditions & MeSH terms

• Hemodialysis

Intervention

Procedure:
• blood sample
blood sample before and after a single HD
• Flow-mediated dilation (FMD) before and after a single HD
measuring of the flow-mediated dilation using high-resolution ultrasound

Locations

Country	Name	City	State
Germany	University Hospital	Aachen	NRW

Sponsors (2)

Lead Sponsor	Collaborator
RWTH Aachen University	Heinrich-Heine University, Duesseldorf

Country where clinical trial is conducted

Germany, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	influence of hemodialysis on endothelial function as determined by plasma nitrite concentration		before and after hemodialysis	No
Secondary	influence on hemodialysis on endothelial function as determined by measurement of flow-mediated dilation (FMD) of teh brachial artery using high resolution ultrasound		before and after hemodialysis	No