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Vitamin-D-Resistant Osteomalacia in Hemodialysis Patients Lacking Secondary Hyperparathyroidism

ANTHONY B. HODSMAN, M.B.; DONALD J. SHERRARD, M.D.; EUGENE G. C. WONG, M.D.; ARNOLD S. BRICKMAN, M.D.; DAVID B. N. LEE, M.D.; ALLAN C. ALFREY, M.D.; FREDERICK R. SINGER, M.D.; ANTHONY W. NORMAN, Ph.D.; and JACK W. COBURN, M.D.
[+] Article and Author Information

Grant support: in part by Grant AM 14750 and Contract AM 72204 from the U. S. Public Health Service and Veterans Administration research funds.

▸Requests for reprints should be addressed to Jack W. Coburn, M.D.; Veterans Administration Wadsworth Medical Center, Sawtelle and Wilshire Blvds.; Los Angeles, CA 90073.


Los Angeles, California; Seattle, Washington; Honolulu, Hawaii; Sepulveda, California; Denver, Colorado; and Riverside, California


© 1981 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1981;94(5):629-637. doi:10.7326/0003-4819-94-5-629
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We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1α, 25-dihydroxycholecalciferol) led to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.

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