Over the past decade important advances in our understanding of the pathophysiology and treatment of renal osteodystrophy have been made. In particular, the role of calcitriol deficiency in the genesis of hyperparathyroidism in early renal failure is now better understood. So too are the effects of aluminium on bone, and whereas the more florid aluminium related disease is now unusual the more subtle effects of aluminium are now being appreciated. There is still a major problem in the long-term treatment of hyperparathyroid bone disease. The reasons why parathyroid gland proliferation continues to occur on dialysis therapy require a better understanding of cellular events regulating hormone production and parathyroid cell replication. The case for early intervention with vitamin D is now strong but whether such an approach materially influences the long-term outcome is not yet established. Changes in the approach to treatment and in the modalities used for renal replacement therapy will continue to modify the nature of the bone disease.