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Vitamin D Intoxication in an Anephric Child

SANDRA JO COUNTS, M.D.; DAVID J. BAYLINK, M.D.; FU-HSIUNG SHEN, M.D.; DONALD J. SHERRARD, M.D.; and ROBERT O. HICKMAN, M.D.
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Grant support: Dr. Counts is a VA research and education trainee. Dr. Baylink is the recipient of Career Development Award DE 19108. Dr. Shen is supported by U.S. Public Health Service training grant TO 1-AM-05221-14. The study was supported in part by U.S. Public Health Service grant AM 09096.

▸Requests for reprints should be addressed to David J. Baylink, M.D., Veterans Administration Hospital, 4435 Beacon Avenue South, Seattle, WA 98108.


Seattle, Washington


Ann Intern Med. 1975;82(2):196-200. doi:10.7326/0003-4819-82-2-196
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Although the biologically active metabolite of vitamin D, 1,25-dihydroxycholecalciferol, is synthesized exclusively by kidney tissue, severe hypercalcemia developed in an anephric child treated with large doses of vitamin D. Treatment by calcium-free peritoneal dialysis acutely reduced serum calcium from 17.2 to 14.2 mg/100 ml. This decrement was effected by removal of three times the total calcium in extracellular fluid, suggesting enhanced bone resorption. Oral prednisolone for 7 days reduced serum calcium to 13 mg/100 ml, but hypercalcemia recurred rapidly after prednisolone was stopped. Calcitonin, given for only 4½ days, produced normocalcemia. Maximum serum 25-hydroxyvitamin D (25-OHD), observed immediately after vitamin D was stopped, was 635 ng/ml (normal range 23-32 ng/ml) and subsequently decreased with an initial half-time of 10 days. Losses in peritoneal dialysate may have contributed to disappearance of serum 25-OHD. Because of the high serum levels of 25-OHD and absence of renal tissue, 25-OHD was the likely metabolite that caused hypercalcemia, probably by stimulation of bone resorption, though contribution to hypercalcemia by another vitamin D metabolite cannot be absolutely excluded.

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