These clinical practices are complicated by the observation that carboxy fragments of PTH (e.g. 7-84) cross react with second generation PTH assays. Because carboxy PTH fragments are either inert or antagonize functional bio-intact PTH (1-84), clinicians have used excessive doses of vitamin D analogues to regulate PTH levels. Moreover, there are animal model studies that suggest that carboxy PTH fragments directly contribute to vascular calcification 16.We propose that clinical decision making using the incomplete information provided the currently available second generation PTH assays leads to excessive vitamin D administration and subsequent acceleration of coronary calcification.