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Robert A. Robinson, MD

Arch Intern Med. 1969;124(5):519-529.

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

Many patients with renal insufficiency have renal osteodystrophy.^1,2 Follis and Jackson ³ found that among 39 adults dying with renal insufficiency, 19 had osteomalacia and 12 had osteitis fibrosa on histologic examination of their skeletons. Many had combined lesions.

Osteomalacia is characterized by bone matrix that can potentially mineralize but hasn't done so.^4,5 For instance, in vivo, long after bone matrix formation (osteoid) has occurred in rachitic animals, that matrix is mineralizable when the cause of the rickets is removed.⁶ As might be expected from the water displacement theory of bone mineralization ^7-9 osteomalacic bone has an abnormally high water content.¹⁰

In renal osteodystrophy, unlike rickets with vitamin D deficiency or a low phosphate value, osteomalacia is not usually due to a low calcium-phosphorus product.¹¹ Usually this product in the patient with chronic renal failure is elevated rather than depressed (Table). There are many theories about the cause of osteomalacia, . . . [Full Text PDF of this Article]

Author Affiliations
Baltimore

From the Division of Orthopedic Surgery, the Johns Hopkins Medical School and the Johns Hopkins Hospital, Baltimore.

Footnotes
Received for publication June 11, 1969; accepted July 17.

Presented at the Conference on Divalent Ion Metabolism and Osteodystrophy in Chronic Renal Failure, Santa Barbara, Calif, Nov 19, 1968.

Reprint requests to Division of Orthopedic Surgery, the Johns Hopkins Medical School and the Johns Hopkins Hospital, Baltimore 21205 (Dr. Robinson).

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