DAWN S. MILLINER, M.D.; HENRY G. NEBEKER, M.D., Ph.D.; SUSAN M. OTT, M.D.; DENNIS L. ANDRESS, M.D.; DONALD J. SHERRARD, M.D.; ALLEN C. ALFREY, M.D.; EDUARDO A. SLATOPOLSKY, M.D.; JACK W. COBURN, M.D.
MILLINER DS, NEBEKER HG, OTT SM, ANDRESS DL, SHERRARD DJ, ALFREY AC, et al. Use of the Deferoxamine Infusion Test in the Diagnosis of Aluminum-Related Osteodystrophy. Ann Intern Med. 1984;101:775-780. doi: 10.7326/0003-4819-101-6-775
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Published: Ann Intern Med. 1984;101(6):775-780.
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.
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Nephrology, Renal Replacement Therapy.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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