Abstract
Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1α,25-dihydroxyvitamin D 3 (1α25(OH)D 3) or 1α,hydroxyvitamin D 3 (1α(OH)D 3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were the serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1α,25(OH) 2D 3 or 1α(OH)D 3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1α,25(OH) 2D 3, play a role in regulating bone formation and/or mineralization.
Published Version
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