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Osteomalacia After Parathyroidectomy in Patients with Uremia

ARNOLD J. FELSENFELD, M.D.; JOHN M. HARRELSON, M.D.; ROBERT A. GUTMAN, M.D.; SAMUEL A. WELLS Jr., M.D.; and MARC K. DREZNER, M.D.
[+] Article and Author Information

Grant support: in part by a grant from the National Institute of Arthritis, Metabolism, and Digestive Diseases (KM 27032-02) and from the March of Dimes Birth Defects Foundation (5-279). Dr. Drezner is the recipient of the Research Career Development Award from the National Institute of Arthritis, Metabolism and Digestive Diseases (AM00643-02).

Presented in part at the meeting of the American Society of Nephrology, 19 November 1979, in Boston, Massachusetts.

▸Requests for reprints should be addressed to Arnold J. Felsenfeld, M.D.; Division of Nephrology, Oklahoma City Veterans Administration Medical Center. 921 NE 13th Street; Oklahoma City, OK 73104.


Durham, North Carolina; and Oklahoma City, Oklahoma


© 1982 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1982;96(1):34-39. doi:10.7326/0003-4819-96-1-34
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Five patients on maintenance dialysis had symptoms of osteomalacia, proven by biopsy, after parathyroidectomy. In all five patients clinical and radiographic manifestations of secondary hyperparathyroidism were present before surgery, and in two patients preoperative biopsy of bone confirmed the existence of osteitis fibrosa. Like previously described patients with osteomalacia all five had multiple fractures and normal or high serum calcium concentrations that rose to abnormally high values on treatment with vitamin D or dihydrotachysterol. Quantitative histomorphometry of biopsy after parathyroidectomy showed no residual parathyroid hormone effect and nearly complete cessation of mineralization. Four patients had forearm autografts of parathyroid tissue that appeared to be functioning at very low rates according to paired venous sampling, and all five patients had relatively low circulating concentrations of parathyroid hormone. This and earlier experiences reported by others suggest that secondary hyperparathyroidism may have an important facilitative role in the mineralization of bone in uremic patients.

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