Vitamin D and Carboxy PTH Fragments in Coronary Calcification
Status:
Withdrawn
Trial end date:
2009-07-01
Target enrollment:
Participant gender:
Summary
Arterial calcification within the coronaries and other vessels is greatly accelerated among
patients with chronic or end-stage kidney disease. The mechanisms leading to increased
calcification are unknown, but include hyperphosphatemia, hyperparathyroidism and altered
vitamin D metabolism. Moreover, recent data demonstrates that circulating carboxy fragments
of PTH (7-84) are physiologic antagonists of intact PTH (1-84) and may directly contribute to
vascular calcification. Current PTH assays no not distinguish between intact and carboxy PTH
fragments leading to an overestimation of intact PTH levels. Because second generation PTH
assays detect both 1-84 and 7-84 PTH fragments, the use of vitamin D analogues to treat
secondary hyperparathyroidism could lead to excessive suppression of 1-84 and a preponderance
of carboxy PTH fragments. Moreover, increased administration of vitamin D analogues amy
contribute to vascular calcifications. To investigate these questions, we plan to investigate
the effect of managing new ESRD patients using conventional and third generation PTH assays
on vitamin D administration and the development of coronary calcification. Hypothesis #1:
Clinical management of secondary hyperparathyroidism in new hemodialysis patients using the
Scantibodies 1-84/7-84 PTH ratio for one year will reduce the amount of Vitamin D
administration resulting in reduced coronary calcification compared to patients in which PTH
management is accomplished by conventional, second generation PTH assay.
Phase:
Phase 4
Details
Lead Sponsor:
Southeast Renal Research Institute
Treatments:
1 alpha-hydroxyergocalciferol Ergocalciferols Vitamin D