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Early skeletal and biochemical alterations in pediatric chronic kidney disease

Katherine Wesseling-Perry1, Renata C Pereira, Chi-Hong Tseng

  • 1Department of Pediatrics, David Geffen School of Medicine at UCLA, A2-383 MDCC, 650 Charles Young Drive, Los Angeles, CA 90095, USA. kwesseling@mednet.ucla.edu

Clinical Journal of the American Society of Nephrology : CJASN
|November 5, 2011
PubMed

Insights

Fibroblast growth factor 23 (FGF-23) and impaired bone mineralization are common in early pediatric chronic kidney disease (CKD). These findings suggest non-traditional factors influence renal bone disease development in children with CKD.

Area of Science:

  • Pediatric Nephrology
  • Mineral Metabolism
  • Bone Biology

Background:

  • The interplay between parathyroid hormone (PTH), fibroblast growth factor 23 (FGF-23), and bone turnover/mineralization in early pediatric chronic kidney disease (CKD) remains unclear.
  • This study aimed to characterize renal osteodystrophy features and their biochemical associations in children with CKD.

Purpose of the Study:

  • To investigate the relationship between parathyroid hormone, FGF-23, and bone turnover/mineralization indices in children with early CKD.
  • To characterize the features of renal osteodystrophy in pediatric CKD patients.

Main Methods:

  • Fifty-two predialysis pediatric CKD patients (2-21 years) underwent tetracycline-labeled bone biopsy.
  • Anthropometric measurements and biochemical parameters were collected at the time of biopsy.

Main Results:

  • Elevated FGF-23 was observed in 81% of all patients, irrespective of CKD stage.
  • Bone turnover was normal in stage 2 CKD but increased in 13% (stage 3) and 29% (stage 4/5) of patients.
  • Defective mineralization was present in 29% (stage 2), 42% (stage 3), and 79% (stage 4/5) of patients, associated with lower calcium and higher PTH levels.

Conclusions:

  • Elevated FGF-23 and early skeletal mineralization defects are prevalent in pediatric CKD.
  • These findings suggest that factors beyond traditional mineral deficiency markers contribute significantly to renal bone disease in children with CKD.
Abstract

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