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Defective Skeletal Mineralization in Pediatric CKD

  • Kidney and Bone (SM Moe and IB Salusky, Section Editors)
  • Published:
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Abstract

Although traditional diagnosis and treatment of renal osteodystrophy focused on changes in bone turnover, current data demonstrate that abnormalities in skeletal mineralization are also prevalent in pediatric chronic kidney disease (CKD) and likely contribute to skeletal morbidities that continue to plague this population. It is now clear that alterations in osteocyte biology, manifested by changes in osteocytic protein expression, occur in early CKD before abnormalities in traditional measures of mineral metabolism are apparent and may contribute to defective skeletal mineralization. Current treatment paradigms advocate the use of 1,25(OH)2vitamin D for the control of secondary hyperparathyroidism; however, these agents fail to correct defective skeletal mineralization and may exacerbate already altered osteocyte biology. Further studies are critically needed to identify the initial trigger for abnormalities of skeletal mineralization as well as the potential effects that current therapeutic options may have on osteocyte biology and bone mineralization.

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K Wesseling Perry has received research support unrelated to this manuscript from the NIH, ASN, Genzyme, Genentech, and the Casey-Lee Ball Foundation.

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All studies by the author involving animal and/or human subjects were performed after approval by the appropriate institutional review boards. When required, written informed consent was obtained from all participants.

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Correspondence to Katherine Wesseling-Perry.

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Wesseling-Perry, K. Defective Skeletal Mineralization in Pediatric CKD. Curr Osteoporos Rep 13, 98–105 (2015). https://doi.org/10.1007/s11914-015-0253-4

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