PURPOSE OF REVIEW Adynamic bone disease has recently been associated with increased risk of vascular calcification. This review focuses on the emerging data in adynamic bone disease, its clinical consequences and therapeutic implications. RECENT FINDINGS There is a lack of good biochemical markers of parathyroid status, bone formation and reabsorption to allow a secure diagnosis of bone disease. Recent data have suggested a possible link between bone activity and vascular calcification. Cardiovascular calcification is an independent predictor of mortality. Adynamic bone is associated with a very low capacity of bone to incorporate calcium in the bone compartment and inability to handle an extra calcium load. A positive association between vascular calcifications and low bone turnover has been suggested. Calcium-containing phosphate binders, active vitamin D therapy and high calcium dialysate may enhance vascular calcifications in the presence of adynamic bone disease. SUMMARY There is recent evidence suggesting a negative impact of calcium load in the progression of vascular calcification in dialysis patients with chronic kidney disease stage 5 with adynamic bone disease. The current therapeutic approach to these patients should focus on reduction of calcium and vitamin D load to restore parathyroid activity.