4.6 Article

Early Skeletal and Biochemical Alterations in Pediatric Chronic Kidney Disease

Journal

Publisher

AMER SOC NEPHROLOGY
DOI: 10.2215/CJN.05940611

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Funding

  1. US Public Health Service [DK-67563, DK-35423, DK-51081, DK-073039, RR-00865]
  2. Casey Lee Ball Foundation
  3. NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR000124] Funding Source: NIH RePORTER
  4. NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000865, UL1RR033176] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK067563, R01DK035423, K23DK080984, R01DK073039, R01DK051081] Funding Source: NIH RePORTER

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Background and objectives The relationship between parathyroid hormone, fibroblast growth factor 23 (FGF-23), and indices of bone turnover and mineralization in children with early CKD is unknown; thus, this study characterizes the features of renal osteodystrophy and their relationship to biochemical markers of mineral metabolism. Design, setting, participants, & measurements Fifty-two patients 2-21 years of age with predialysis CKD underwent tetracycline-labeled bone biopsy. Anthropomorphic measurements and biochemical values were obtained at the time of biopsy. Results Serum phosphorus levels were increased in 4% of patients with stage 3 CKD and 43% of those with stage 4/5 CKD. Parathyroid hormone concentrations were elevated in 36% of patients with stage 2, 71% with stage 3, and 93% with stage 4/5 CKD, whereas FGF-23 values were elevated in 81% of all patients, regardless of CKD stage. Bone turnover was normal in all patients with stage 2, but was increased in 13% with stage 3 and 29% with stage 4/5 CKD. Defective mineralization was present in 29% of patients with stage 2, 42% with stage 3, and 79% with stage 4/5 CKD. Defective skeletal mineralization was associated with lower serum calcium levels and increased parathyroid hormone concentrations. Conclusions Elevated circulating FGF-23 levels and defects in skeletal mineralization early in the course of CKD suggest that factors other than the traditional markers of mineral deficiency play a crucial role in the development of renal bone disease. Clin J Am Soc Nephrol 7: 146-152, 2012. doi: 10.2215/CJN.05940611

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