Secondary hyperparathyroidism is a metabolic state characterized by an excessive but not autonomous rate of production of parathyroid hormone: this disorder is encountered invariably in chronic renal failure and also in other disease states where there is resistance to the metabolic actions of parathyroid hormone.1 The resistance to the biological effects of the hormone lead, through mechanisms as yet unclarified, to hyperplasia of the parathyroids. For many years secondary hyperparathyroidism had been postulated to be present in patients with chronic renal disease.2 It was known from postmortem studies of patients with renal failure that the parathyroids were hyperplastic; in addition, changes typical of osteitis fibrosa were found in many patients with far advanced renal failure, as discussed elsewhere in this symposium by Stanbury and others. Studies with the radioimmunoassay by Berson and Yalow, Reiss (reviewed in this symposium), and us have now confirmed that there is an increased concentration of
Potts JT, Reitz RE, Deftos LJ, et al. Secondary Hyperparathyroidism in Chronic Renal Disease. Arch Intern Med. 1969;124(4):408–412. doi:10.1001/archinte.1969.00300200020003
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