Chronic kidney disease and especially end-stage renal disease (ESRD) are regularly associated with profound disturbances in the mineral metabolism characterized by secondary hyperparathyroidism (SHPT), hyperphosphatemia, hypercalcemia, elevated calcium-phosphorus product and renal osteodystrophy. These metabolic changes are either the result of the disease itself or due to toxicity from current therapeutic options. There is growing evidence that besides the classical cardiovascular risk factors, non-traditional uremia-specific risk factors, including abnormal mineral metabolism and SHPT, play a key role in the excessively increased cardiovascular mortality and morbidity in these patients. Calcimimetics represent an innovative new therapeutic compound in the treatment of SHPT, acting as allosteric activators of the calcium-sensing receptor. In this review we will discuss the consequences of SHPT in ESRD patients on vascular calcification, its impact on cardiovascular morbidity and mortality and the potential role of calcimimetics in preventing the cardiovascular consequences of SHPT.