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Research Article Free access | 10.1172/JCI107558
University of Washington, Department of Medicine, Seattle, Washington 98195
Veterans Administration Hospital, Seattle, Washington 98195
Find articles by Burneli, J. in: JCI | PubMed | Google Scholar
University of Washington, Department of Medicine, Seattle, Washington 98195
Veterans Administration Hospital, Seattle, Washington 98195
Find articles by Teubner, E. in: JCI | PubMed | Google Scholar
University of Washington, Department of Medicine, Seattle, Washington 98195
Veterans Administration Hospital, Seattle, Washington 98195
Find articles by Wergedal, J. in: JCI | PubMed | Google Scholar
University of Washington, Department of Medicine, Seattle, Washington 98195
Veterans Administration Hospital, Seattle, Washington 98195
Find articles by Sherrard, D. in: JCI | PubMed | Google Scholar
Published January 1, 1974 - More info
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.