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Research Article Free access | 10.1172/JCI107558

Bone Crystal Maturation in Renal Osteodystrophy in Humans

James M. Burneli, Elizabeth Teubner, Jon E. Wergedal, and Donald J. Sherrard

University of Washington, Department of Medicine, Seattle, Washington 98195

Veterans Administration Hospital, Seattle, Washington 98195

Find articles by Burneli, J. in: PubMed | Google Scholar

University of Washington, Department of Medicine, Seattle, Washington 98195

Veterans Administration Hospital, Seattle, Washington 98195

Find articles by Teubner, E. in: PubMed | Google Scholar

University of Washington, Department of Medicine, Seattle, Washington 98195

Veterans Administration Hospital, Seattle, Washington 98195

Find articles by Wergedal, J. in: PubMed | Google Scholar

University of Washington, Department of Medicine, Seattle, Washington 98195

Veterans Administration Hospital, Seattle, Washington 98195

Find articles by Sherrard, D. in: PubMed | Google Scholar

Published January 1, 1974 - More info

Published in Volume 53, Issue 1 on January 1, 1974
J Clin Invest. 1974;53(1):52–58. https://doi.org/10.1172/JCI107558.
© 1974 The American Society for Clinical Investigation
Published January 1, 1974 - Version history
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Abstract

Calcium, phosphorus, sodium, carbonate, magnesium, and hydroxyproline were measured in iliaccrest biopsies of 22 normal volunteers and 24 selected patients with renal osteodystrophy. Histologic classification revealed that 10 were mildly abnormal, 8 osteomalacic, and 6 osteofibrotic. Bone density measurements were performed on an additional 12 normal, 11 mildly abnormal, 6 osteomalacic, and 10 osteofibrotic subjects. The results revealed an increase in magnesium and adecrease in carbonate apparent in the minimal and osteomalacic lesions and a much greater change in osteofibrosis. The bone density was decreased in patients with osteofibrosis. These observations would appear to be explained by postulation of an impairment of the normal maturational process of bone whereby there is an increase in amorphous calcium phosphate and a decrease in apatite crystal. The data suggest that the maturational defect is present as soon as any abnormality can be identified histologically, is present to the same degree in osteomalacia, and is most severe in osteofibrosis. In comparison of two sets of six patients matched for age and duration of dialysis, neither acidosis nor vitamin D therapy appeared to influence the severity of the maturational defect.

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