Clinical trial NCT00764192: Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries
Official title: Angiologic Study of the Influence of Hemodialysis on Endothelial Function
Study type: INTERVENTIONAL
Overall status: COMPLETED
Phase: NA
Conditions: Hemodialysis
Keywords: hemodialysis
Flow-mediated dilation
nictric oxide
endothelial function
Lead sponsor: RWTH Aachen University
Sponsor class: OTHER
Collaborators: name: Heinrich-Heine University, Duesseldorf
First posted: 2008-10-01
Enrollment: 14
Sex: ALL
Minimum age (years): 21
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Allocation: NA
Intervention model: SINGLE_GROUP
Primary purpose: BASIC_SCIENCE

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

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

Primary outcomes:
measure: influence of hemodialysis on endothelial function as determined by plasma nitrite concentration
timeFrame: before and after hemodialysis
Secondary outcomes:
measure: influence on hemodialysis on endothelial function as determined by measurement of flow-mediated dilation (FMD) of teh brachial artery using high resolution ultrasound
timeFrame: before and after hemodialysis
Other outcomes:
Locations:
city: Aachen
country: Germany
facility: University Hospital
state: NRW
Study officials:
affiliation: RWTH Aachen University, Medical Clinic I
name: Christian Meyer, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: 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.