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1,25-Dihydroxyvitamin D3 in the Treatment of Juvenile Renal Osteodystrophy

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Pediatric Nephrology

Part of the book series: Developments in Nephrology ((DINE,volume 3))

Abstract

The discovery of the vitamin D-endocrine system and the finding that the kidney is a major site of the synthesis of vitamin D metabolites, provides a theoretical explanation for the vitamin D resistance of uremic osteodystrophy (1). Calcitriol (1,25(OH)2D) and 24,25(OH)2D are predominately synthesized in mitochondria of proximal tubule cells. Because of the reduction in nephron mass in uremia, the synthesis of these metabolites is impaired and circulating levels are low (2). A reduction in calcitriol levels, and possibly in those of 24,25(OH)2D, results in diminished gut calcium absorption, secondary hyperparathyroidism and undermineralized osteoid and growing surfaces of bone (3). Ultimately, uremic children develop widened growth plates, bone age retardation and growth failure.

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Authors and Affiliations

  1. Dept. of Pediatrics, Univ. of Wisconsin, Madison, WI, USA

    Russell W. Chesney

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  1. Russell W. Chesney
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Editors and Affiliations

  1. St. Christopher’s Hospital for Children, Philadelphia, PA, USA

    Alan B. Gruskin MD (President) (President)

  2. Section of Nephrology, Children’s Hospital of Philadelphia, 34th and Civic Center Boulevard, Philadelphia, PA, 19104, USA

    Michael E. Norman MD (Secretary General) (Secretary General)

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© 1981 Martinus Nijhoff Publishers, The Hague

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Chesney, R.W. (1981). 1,25-Dihydroxyvitamin D3 in the Treatment of Juvenile Renal Osteodystrophy. In: Gruskin, A.B., Norman, M.E. (eds) Pediatric Nephrology. Developments in Nephrology, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-8319-9_28

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  • DOI: https://doi.org/10.1007/978-94-009-8319-9_28

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-009-8321-2

  • Online ISBN: 978-94-009-8319-9

  • eBook Packages: Springer Book Archive

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