Derangements of mineral metabolism occur during the early stages of chronic kidney disease (CKD). Hyperphosphatemia develops in the majority of patients with ESRD and has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy. More recent observational data have associated hyperphosphatemia with increased cardiovascular mortality among dialysis patients. Adequate control of serum phosphorus remains a cornerstone in the clinical management of patients with CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduce the risk for vascular calcification and cardiovascular mortality. These measures include dietary phosphorus restriction, dialysis, and oral phosphate binders. Dietary restriction is limited in advanced stages of CKD. Phosphate binders are necessary to limit dietary absorption of phosphorus. Aluminum hydroxide is an efficient binder; however, its use has been nearly eliminated because of concerns of toxicity. Calcium salts are inexpensive and have been used effectively worldwide as an alternative to aluminum. Concerns of calcium overload have led to the investigation of alternatives. Currently, only two Food and Drug Administration-approved noncalcium, nonaluminum binders are available. Sevelamer hydrochloride is an exchange resin and was not as effective as calcium acetate in meeting new guideline recommendations in one double-blind clinical trial. Lanthanum carbonate is a rare earth element and has been studied less extensively. Concerns of long-term administration and toxicity exist. Furthermore, these agents are significantly more expensive than calcium salts, which may contribute to patient noncompliance.