Early Skeletal and Biochemical Alterations in Pediatric Chronic Kidney Disease

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 meta...

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Published inClinical journal of the American Society of Nephrology Vol. 7; no. 1; pp. 146 - 152
Main Authors Wesseling-Perry, Katherine, Pereira, Renata C, Tseng, Chi-Hong, Elashoff, Robert, Zaritsky, Joshua J, Yadin, Ora, Sahney, Shobha, Gales, Barbara, Jüppner, Harald, Salusky, Isidro B
Format Journal Article
LanguageEnglish
Published United States American Society of Nephrology 01.01.2012
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Summary: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. 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. 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. 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.
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ISSN:1555-9041
1555-905X
DOI:10.2215/CJN.05940611