Cardiovascular disease (CVD) remains the major mortality risk in dialysis patients, accounting for almost 50 percent of deaths. Risk is related to the increased prevalence of traditional risk factors for CVD and to the contribution of abnormalities in mineral metabolism as well as cardiovascular calcification. Hyperphosphatemia invariably is present among patients with end-stage renal disease and is becoming an increasingly important clinical entity. In addition to its role in the pathogenesis of secondary hyperparathyroidism, elevated serum phosphorus increases the mortality risk among these patients. The pathophysiologic mechanisms by which persistent hyperphosphatemia enhances mortality risk in dialysis patients are not yet completely understood. Given that inadequate control of serum phosphorus contributes to elevated calcium-phosphorus (Ca x P) product, hyperphosphatemia may play a key role in cardiovascular calcification. The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (K/DOQI) "Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease" recommends more stringent levels for controlling serum phosphorus and Ca x P product to improve patients' quality of life and longevity. Several studies, including the CARE study, have shown that calcium acetate is more cost-effective than sevelamer as a phosphate binder. Although concern has been raised about its purported link to cardiovascular calcification, the author demonstrates in this review that calcium acetate can be used effectively with doses of elemental calcium that meet the K/DOQI guidelines.