Arterial Stiffness and Decreased Bone Buffering Capacity in Hemodialysis Patients
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT00485706|
Recruitment Status : Completed
First Posted : June 13, 2007
Last Update Posted : January 18, 2010
Renal patients have an increased risk for cardiovascular complications. There is also increased vascular calcification and bone metabolism is similarly abnormal in patients with chronic kidney disease.
In dialysis patients frequent episodes of hypercalcaemia occur. In a healthy bone structure those episodes of hypercalcemia are buffered by the bone. The absence of bone buffering capacity in dialysis patients can be a mechanism for vascular calcifications.
|Condition or disease||Intervention/treatment|
|Kidney Disease Hypercalcemia||Procedure: high calcium dialysate|
Patient with a higher ∆ Calcium (Calcium post - Calcium pre) have a diminished bone buffering capacity indicative for adynamic bone disease compared with patients with smaller ∆ Calcium.
This may result in higher extraosseous calcification and higher pulse wave velocity
∆ PTH/∆ Calcium may reflect the sensitivity and density of the calcium receptors; this may reflect parathyroid "health"
|Study Type :||Interventional (Clinical Trial)|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Arterial Stiffness and Decreased Bone Buffering Capacity in Hemodialysis Patients|
|Study Start Date :||June 2007|
- correlation between calcium increase and pulse wave velocity
- correlation between calcium change and pth change
- correlation between calcium increase and vascular calcifications
- correlation between calcium change and bone markers
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00485706
|LEuven, Belgium, 3000|
|Principal Investigator:||kathleen Claes, MD||UZ Gasthuisberg|