1,25 Dihydroxycholecalciferol Effects in Chronic Dialysis

doi:10.1059/0003-4819-88-6-774

1,25 Dihydroxycholecalciferol Effects in Chronic Dialysis

A Double-Blind Controlled Study

TOMAS BERL, M. D.;
ARNOLD S. BERNS, M.D.;
WILLIAM E. HUFFER, M.D.;
KAREN HAMMILL, R.N.;
ALLEN C. ALFREY, M.D., F.A.C.P.;
CLAUDE D. ARNAUD, M.D., F.A.C.P.; and
ROBERT W. SCHRIER, M.D., F.A.C.P.

Denver, Colorado, and Rochester, Minnesota

Abstract

1,25 dihydroxycholecalciferol [1,25(OH)₂D₃] was studied in a double-blind controlled fashion in patients on chronic dialysis. Serum calcium was unchanged in 16 patients on vitamin D₃(D₃) (400 to 1200 IU/day). In 15 patients on 1,25(OH)₂D₃ (0.5 to 1.5 µg/day), serum calcium increased from 9.05 ± .15 to 10.25 ± .20 mg/dl (_p < 0.001), returning to 9.37 ± .16 mg/dl (_p < 0.001) in the post control period. Patients on D₃ showed no reversible decrease in immunoreactive parathyroid hormone levels, but patients on 1,25(OH)₂D₃ did, from a control of 1077 ± 258 to 595 ± 213 µl equivalents/ml (p < 0.01), and returned to 1165 ± 271 µl equivalents/ml (p < 0.005). Nine of 12 patients on D₃ who underwent serial iliac-crest biopsies showed histologic deterioration, and six of seven who received 1,25(OH)₂D₃ were improved or unchanged (p < 0.025). Bone mineral and calcium decreased in patients on D₃ (p < 0.05) but not in those on 1,25(OH)₂D₃. Hypercalcemia occurred in five of 15 patients. We conclude that 1,25(OH)₂D₃ has a calcemic effect in chronic dialysis patients, decreases levels of immunoreactive parathyroid hormone, and is associated with histologic improvement in bone disease. Thus, 1,25(OH)₂D₃ is a valuable adjunct to the management of renal osteodystrophy but requires monitoring of serum calcium to avoid hypercalcemia.

Article and Author Information

▸From the Departments of Medicine and Pathology, University of Colorado Medical Center; Denver, Colorado; and the Department of Medicine, Mayo Clinic; Rochester, Minnesota.
Grant support: by a grant from the General Clinical Research Center Program of the Division of Research Resource, National Institutes of Health (RR-00051); a research grant from the National Institutes of Health (HL 15629); and a grant from the Hoffmann-La Roche Company. Dr. Arnold S. Berns was supported by a research fellowship grant from the Rocky Mountain Kidney Foundation.
▸Requests for reprints should be addressed to Tomas Berl, M.D.; Box C-281, University of Colorado Medical Center; 4200 East 9th Avenue; Denver, CO 80262.
- Received September 16, 1977.
- Accepted February 13, 1978.