Use of the Deferoxamine Infusion Test in the Diagnosis of Aluminum-Related Osteodystrophy

doi:10.1059/0003-4819-101-6-775

Use of the Deferoxamine Infusion Test in the Diagnosis of Aluminum-Related Osteodystrophy

Los Angeles, California; Seattle, Washington; Denver, Colorado; and St. Louis, Missouri

Abstract

The accumulation of aluminum in bone can cause disabling osteodystrophy in patients with renal failure. Because the chelating agent deferoxamine can mobilize aluminum from tissues, we evaluated the effect of a standard intravenous dose of deferoxamine on plasma aluminum concentrations in 54 patients on hemodialysis. Stainable bone aluminum, bone histologic findings, and bone aluminum content were studied. Baseline plasma aluminum concentrations of greater than 200 µg/L were associated with aluminum-related osteodystrophy (specificity, 93%), but concentrations of less than 200 µg/L did not exclude the diagnosis (sensitivity, 43%). After administration of deferoxamine, the increase in plasma aluminum concentration was 534 ± 260 (SD) and 214 ± 92 µg/L in patients with and without aluminum-related bone disease, respectively (p < 0.001), and correlated with the bone aluminum content (r = 0.64). An increment in plasma aluminum concentration of greater than 200 µg/L identified 35 of the 37 patients with aluminum-related osteodystrophy; sensitivity was 94% and specificity, 50%. The deferoxamine infusion test is noninvasive, well tolerated, and of value particularly in excluding the diagnosis of aluminum-related osteodystrophy.

Article and Author Information

▸From the Medical and Research Services, Veterans Administration Wadsworth Medical Center, and Department of Medicine, UCLA School of Medicine, Los Angeles, California; Division of Nephrology, Harborview Medical Center, Medical and Research Services, Veterans Administration Medical Center, and University of Washington School of Medicine, Seattle, Washington; Medical and Research Services, Veterans Administration Medical Center, and University of Colorado School of Medicine, Denver, Colorado; and Washington University School of Medicine, St. Louis, Missouri.
Grant support: in part by grants AM-14750, AM-29926, AM-9976, and AM-7126; from the National Institutes of Health, Public Health Service, and by General Clinical Research Center Grants RR-37 (CLINFO computer system) and RR-865. Dr. Milliner was a Mayo Foundation Scholar at the Wadsworth Veterans Administration Medical Center at the time of the study. Dr. Coburn is a Medical Investigator of the Veterans Administration.
▸Requests for reprints should be addressed to Dawn S. Milliner, M.D.; Division of Nephrology and Internal Medicine, Mayo Clinic, Rochester, MN 55905.