The wide spectrum of metabolic bone disease that occurs during the course of advancing renal insufficiency has been well documented in the recent literature.1 At one end of the spectrum, the predominant skeletal abnormality is osteomalacia with defective mineralization of osteoid. At the other end of the spectrum, there is osteitis fibrosa. Between these extremes, many variations and combinations of metabolic bone disease occur.
In the early 1960's, Dent et al2 and Stanbury and Lumb 3 independently confirmed and extended the neglected observations of Liu and Chu in 1943,4 according to which calcium malabsorption was a prominent feature of renal failure. Dent et al and Stanbury and Lumb documented the vitamin D-resistant state in renal failure and showed that the osteomalacic bone disease is curable by administration of adequate amounts of vitamin D. More recently, Avioli et al 5 demonstrated that abnormal metabolism of vitamin D in