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Is There a Controversy?

Shaul G. Massry, MD; Eberhard Ritz, MD

Arch Intern Med. 1978;138(Suppl 5):853-856.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Hyperplasia of the parathyroid glands and elevated blood levels of parathyroid hormone (PTH) are almost always present in patients with chronic renal failure.^1-6 The evidence of this secondary hyperparathyroidism is found even with mild renal insufficiency.⁵ Therefore, the mechanism(s) underlying this abnormality must be operative in the early stages of renal disease.

MECHANISMS OF HYPOCALCEMIA OF RENAL FAILURE

All investigators agree that the stimulus for the hyperplasia of parathyroid glands in these patients is hypocalcemia. A great deal of effort has been devoted to investigate the mechanism(s) of the hypocalcemia of renal failure. At present, two postulates have been advanced. These include phosphate retention^7,8 and skeletal resistance to the calcemic action of PTH.^9-14 The proponents of these two notions have provided evidence supporting their concepts. The vigor with which this has been done perpetuated the impression that these two theories are mutually exclusive and, as such, . . . [Full Text PDF of this Article]

Author Affiliations

Footnotes

Reprint requests to Division of Nephrology, University of Southern California, School of Medicine, 2025 Zonal Ave, Los Angeles, CA 90033 (Dr Massry).

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