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The Clinical Spectrum in Uremia, During Hemodialysis, and After Renal Transplantation

Shaul G. Massry, MD; Jack W. Coburn, MD; Mordecai M. Popovtzer, MD; James H. Shinaberger, MD; Morton H. Maxwell, MD; Charles R. Kleeman, MD

Arch Intern Med. 1969;124(4):431-441.

	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 high levels of circulating parathyroid hormone are common in patients with chronic renal failure,¹ and even in those with mild impairment of renal function.² However, the syndrome of overt hyperparathyroidism is not frequently seen in these patients. With the prolongation of the life of patients with chronic renal failure, overt hyperparathyroidism is being observed with increasing frequency. The exact pathogenetic factors which underlie the dynamics of the processes leading to hyperplasia and hyperactivity of the parathyroid glands, the reasons why overt hyperparathyroidism is not always present, the clinical and biochemical criteria of this entity, and the functional characteristics of the parathyroid glands in patients with chronic uremia during hemodialysis and after renal transplant are as yet not clearly delineated.^3,4

In this report, the term hyperparathyroidism is used to indicate a syndrome with certain clinical, roentgenographic, and biochemical manifestations which are observed . . . [Full Text PDF of this Article]

Author Affiliations

From the Cedars-Sinai Medical Research Institute and departments of medicine, Cedars-Sinai Medical Center (Drs. Massry, Popovtzer, Maxwell, and Kleeman), Veterans Administration Center (Drs. Coburn and Shinaberger), and; UCLA School of Medicine, Los Angeles.

Footnotes

Read before the Conference on Divalent Ion Metabolism and Osteodystrophy in Chronic Renal Failure, Santa Barbara, Calif, Nov 18, 1968.

Reprint requests to 8720 Beverly Blvd, Los Angeles 90048 (Dr. Massry).

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