Controlling serum phosphorus levels continues to be a challenge in patients with chronic renal disease. Hyperphosphatemia is implicated in the development and worsening of secondary hyperparathyroidism and renal osteodystrophy (ROD) through its effects on serum calcium and calcitriol levels, parathyroid hormone (PTH) overproduction, and parathyroid cell hyperplasia. In the past serum phosphorus control with aluminum-containing phosphate binders was associated with insidious but serious development of aluminum toxicity. More recent approaches using non aluminum-containing calcium salts as phosphate binders are limited because of the excessive calcium load resulting from concomitant enhanced intestinal calcium absorption. Moreover serum phosphorus does not only result from dietary phosphate intake but also from enhanced bone breakdown due to secondary hyperparathyroidism. Strategies for managing ROD including early control of serum phosphorus and PTH, prevention of parathyroid hyperplasia; establishment of optimal PTH levels for bone health, and the availability of new therapeutic tools for controlling phosphorus may help prevent complications and improve patient outcomes.