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November 1969

Distortions of Bone Cell Metabolism in Uremia and Their Cause

Author Affiliations


From the Department of Medicine, Harvard Medical School, and Peter Bent Brigham and Boston City hospitals, Boston. Dr. van der Sluys Veer is now with the Department of Endocrinology, Academisch Ziekenhuis Leiden, the Netherlands.

Arch Intern Med. 1969;124(5):530-538. doi:10.1001/archinte.1969.00300210012002

Four features of the uremic syndrome have been implicated as the cause of the skeletal changes which invariably occur in patients with prolonged chronic renal failure: metabolic acidosis,1,2 retention of phosphate (and other ions), functional vitamin D deficiency,3 and secondary hyperparathyroidism.4 Yet, despite extensive investigation we are still unsure about the ultimate causes of renal osteodystrophy and are equally uncertain whether the skeletal response to chronic renal failure is detrimental or whether it represents evidence of a set of compensatory adjustments without which the patient would be even more threatened.

In this communication, we shall review the evidence bearing on these questions which we have accumulated from our studies of bone cell metabolism in vitro. First, we will report the distortions of normal bone cell metabolic patterns observed in biopsy samples taken from 11 uremic patients and show how these patterns resemble those found in patients with

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