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Calcium Metabolism and Osteodystrophy After Renal Transplantation
Constantine L. Hampers, MD;
Adrian I. Katz, MD;
Richard E. Wilson, MD;
John P. Merrill, MD
Arch Intern Med. 1969;124(3):282-291.
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THAT uremia is associated with an abnormal calcium metabolism has been known for some time.1,2 The severity and extent of this defect, however, has become more evident since the introduction of chronic hemodialysis and renal homotransplantation.3,4 These procedures, by prolonging the life of patients with chronic renal failure, have sometimes resulted in an exaggeration of the bone abnormalities whose clinical implications begin only now to be fully appreciated.
The responsiveness of the uremic parathyroid gland to changes in serum calcium concentration has not been completely defined. With persistent stimulation by long-standing hypocalcemia, the hyperplastic glands may become insensitive to the usual stimuli that regulate their secretion. This state of parathyroid "autonomy" produces persistent hypercalcemia and continued hyperparathyroidism and often becomes manifest when the uremia is rapidly corrected by dialysis or transplantation.5,6 With these considerations in mind, this communication is intended to document the biochemical, roentgenological, clinical,
. . . [Full Text PDF of this Article]
Author Affiliations
Boston
From the departments of medicine and surgery, Peter Bent Brigham Hospital and Harvard Medical School, Boston.
Footnotes
Received for publication April 21, 1969; accepted April 23.
Read before the Conference on Divalent
Ion Metabolism and Osteodystrophy in Chronic Renal Failure, Santa Barbara, Calif, Nov 18, 1968.
Reprint requests to Dialysis Facilities, Peter Bent Brigham Hospital, 721 Huntington Ave, Boston 02115 (Dr. Hampers).
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