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Renal Osteodystrophy, Soft Tissue Calcification, and Disturbed Divalent Ion Metabolism in Chronic Renal Failure

Charles R. Kleeman, MD; Shaul G. Massry, MD; Jack W. Coburn, MD; Mordecai M. Popovtzer, MD

Arch Intern Med. 1969;124(3):262-268.

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

For many decades it has been known that there is a close relationship between renal disease, osseous changes, and "parathyroid hyperfunction," or hyperplasia of the parathyroid glands.^1-4 However, due to the apparent infrequency of clinically demonstrable bone disease, serious attention was not paid to this problem in the United States until the excellent British studies of Stanbury⁵ and Dent et al⁶ appeared. Although not conclusively demonstrated, it seemed that the incidence of renal osteodystrophy together with chronic renal failure was considerably greater in the British Isles than in the United States. It is probable that in the last years of World War II and early postwar period in England, the diet was somewhat deficient in calcium, phosphorus, and vitamin D (absence of fortified dairy products); in addition, the amount of sunlight and ultraviolet exposure is probably significantly less than in most areas of the United States. If . . . [Full Text PDF of this Article]

Author Affiliations

From the departments of medicine, Cedars-Sinai Medical Center (Drs. Kleeman, Massry, and Popovtzer); Veterans Administration Center (Dr. Coburn); and UCLA School of Medicine, Los Angeles. Dr. Massry is an established investigator of the American Heart Association.

Footnotes

Also participating were the following cooperative members of Public Health Service Study on Renal Osteodystrophy (PH 43-68-1040): Morton H. Maxwell, MD, Arthur Gordon, MD, Stanley S. Franklin, MD, Dwight L. Makoff, MD, Marshal Fichman, MD, and John De Palma, MD (Cedars-Sinai Medical Center); Milton E. Rubini. MD, and James H. Shinaberger, MD (Veterans Administration Center); Harvey C. Gonick, MD, and Ralph Goldman, MD (UCLA Medical Center); Richard J. Glassock, MD (Harbor General Hospital); and John E. Bethune, MD (USC School of Medicine), Los Angeles.

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. Kleeman).

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