Robert W. Hedger, MD; Eberechukwu Ibe, MD; Arleen French, BS, PA
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Hedger RW, Ibe E, French A. Hypercalcemia after 1,25-Dihydroxyvitamin D3 Production in an End-Stage Kidney. Ann Intern Med. 2003;138:522-523. doi: 10.7326/0003-4819-138-6-200303180-00032
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Published: Ann Intern Med. 2003;138(6):522-523.
TO THE EDITOR:
Background: The physiologic characteristics of vitamin D are well documented. Final hydroxylation in the kidney, by 1-α hydroxylase, forms the active metabolite 1,25-dihydroxyvitamin D3 (vitamin D3) (1, 2). Vitamin D3 production decreases as the glomerular filtration rate falls below 30 mL/min per 1.73 m2. In failed kidneys, vitamin D3 production ceases and serum levels approach zero (3). Macrophages may produce small amounts of vitamin D3, and granulomatous diseases and malignant lymphoma cells can produce enough vitamin D3 to cause hypercalcemia (4-7).
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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