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.