J. H. Felts, M.D., F.A.C.P.; H. H. Bradshaw, M.D.; D. D. Anderson, M.D.; J. E. Whitley, M.D.
Felts JH, Bradshaw HH, Anderson DD, Whitley JE. Management of Azotemic Osteodystrophy.. Ann Intern Med. 1964;60:737. doi: 10.7326/0003-4819-60-4-737_1
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Published: Ann Intern Med. 1964;60(4):737.
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Azotemic osteodystrophy results from secondary hyperparathyroidism and is manifested by typical bony changes, an elevated alkaline phosphatase and, often, a high normal serum calcium concentration. With progression, bone pain and spontaneous fractures lead to skeletal deformity and invalidism. Treatment with oral alkali is ineffective but vitamin D in oral doses to 200,000 units daily usually relieves symptoms within 6 weeks and induces recalcification of bone. Hypervitaminosis D becomes a constant threat to renal function during therapy but skeletal symptoms recur quickly when calciferol is discontinued.
In November, 1960, a 38-year-old woman with azotemia, elevated serum alkaline phosphatase and radiographically classical
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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