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Eric Reiss, MD; Janet M. Canterbury, MS; Alan Kanter, MD

Arch Intern Med. 1969;124(4):417-422.

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

The wide spectrum of metabolic bone disease that occurs during the course of advancing renal insufficiency has been well documented in the recent literature.¹ At one end of the spectrum, the predominant skeletal abnormality is osteomalacia with defective mineralization of osteoid. At the other end of the spectrum, there is osteitis fibrosa. Between these extremes, many variations and combinations of metabolic bone disease occur.

In the early 1960's, Dent et al² and Stanbury and Lumb ³ independently confirmed and extended the neglected observations of Liu and Chu in 1943,⁴ according to which calcium malabsorption was a prominent feature of renal failure. Dent et al and Stanbury and Lumb documented the vitamin D-resistant state in renal failure and showed that the osteomalacic bone disease is curable by administration of adequate amounts of vitamin D. More recently, Avioli et al ⁵ demonstrated that abnormal metabolism of vitamin D in . . . [Full Text PDF of this Article]

Author Affiliations

From the Department of Medicine, Michael Reese Hospital and Medical Center, Chicago.

Footnotes

Read before the Conference on Divalent

Ion Metabolism and Osteodystrophy in Chronic Renal Failure, Santa Barbara, Calif, Nov 18, 1968.

Reprint requests to 2929 S Ellis Ave, Chicago 60616 (Dr. Reiss).

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