As is apparent from the preceding discussion, renal osteodystrophy is a complex entity with multiple causes and many manifestations. Significant problems have included the identification and management of the various forms of bone disease seen in uremia. The prevention and therapy of osteitis fibrosa and secondary hyperparathyroidism have been significantly improved as a result of adequate phosphate restriction and the use of active forms of vitamin D (primarily calcitriol in the U.S., dihydrotachysterol and 1 alpha-hydroxyvitamin D in Europe). Recently, a major problem has been the recognition of bone disease due to aluminum accumulation. The therapy of this bone disease was generally unsuccessful until recent preliminary data suggested that deferoxamine therapy may be useful in these patients. The study of renal osteodystrophy has certainly advanced our knowledge of mineral metabolism, with clarification of the metabolism and action of PTH and vitamin D metabolism and identification of the pathogenic role for aluminum. In the future, most manifestations of renal osteodystrophy may be preventable or adequately treated.