DUNCAN A. MCINTOSH; EMIL W. PETERSON; JOHN J. MCPHAUL JR.
Secondary hyperparathyroidism occurs commonly in chronically uremic patients (1-4). It has been felt to represent a physiologic adjustment to the hypocalcemia that results from impaired gastrointestinal absorption of calcium and renal phosphorus retention (5, 6). Although it appears to evolve as a compensating homeostatic mechanism, the hyperparathyroidism may lead to disabling symptomatology requiring vigorous medical or surgical therapy (5, 7-9). Indeed, the sequelae of the hyperparathyroid state may overshadow other symptoms of the uremia. It has been suggested that these hyperplastic parathyroid glands may lose their homeostatic role and that occasionally an autonomous state of hyperparathyroidism may develop (7, 10,
MCINTOSH DA, PETERSON EW, MCPHAUL JJ. Autonomy of Parathyroid Function After Renal Homotransplantation. Ann Intern Med. 1966;65:900–907. doi: https://doi.org/10.7326/0003-4819-65-5-900
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Published: Ann Intern Med. 1966;65(5):900-907.
Endocrine and Metabolism, Nephrology, Parathyroid Disorders.
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