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Research Article Free access | 10.1172/JCI107134
Department of Medicine, The Jewish Hospital of St. Louis, Missouri 63110
Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Russell, J. in: JCI | PubMed | Google Scholar
Department of Medicine, The Jewish Hospital of St. Louis, Missouri 63110
Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Avioli, L. in: JCI | PubMed | Google Scholar
Published December 1, 1972 - More info
The effect of chronic renal disease on bone matrix and mineral maturation was evaluated in rats with experimental renal insufficiency of 2-11 wk duration utilizing bromoform-toluene gradient fractionation of bone powder, pulse labeling experiments with 45Ca and proline-3H differential extraction, and X-ray diffraction techniques.
Maturation defects in both collagen and mineral (45Ca) metabolism were documented as early as 2 wk after the induction of uremia, when total bone calcium, inorganic phosphate, and hydroxyproline content were unchanged. The maturational defect progressed with advancing uremia despite insignificant changes in plasma pH and calcium, and normal bone carbonate levels.
Although circulating levels of 25-hydroxycholecalciferol were significantly lower than normal in the uremic animals, pretreatment with either this vitamin D metabolite or vitamin D3 itself failed to alter the observed changes in skeletal maturation.