Treatment of Pediatric Chronic Kidney Disease-Mineral and Bone Disorder

Curr Osteoporos Rep. 2017 Jun;15(3):198-206. doi: 10.1007/s11914-017-0365-0.

Abstract

Purpose of review: In this paper, we review the pathogenesis and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD), especially as it relates to pediatric CKD patients.

Recent findings: Disordered regulation of bone and mineral metabolism in CKD may result in fractures, skeletal deformities, and poor growth, which is especially relevant for pediatric CKD patients. Moreover, CKD-MBD may result in extra-skeletal calcification and cardiovascular morbidity. Early increases in fibroblast growth factor 23 (FGF23) levels play a key, primary role in CKD-MBD pathogenesis. Therapeutic approaches in pediatric CKD-MBD aim to minimize complications to the growing skeleton and prevent extra-skeletal calcifications, mainly by addressing hyperphosphatemia and secondary hyperparathyroidism. Ongoing clinical trials are focused on assessing the benefit of FGF23 reduction in CKD. CKD-MBD is a systemic disorder that has significant clinical implications. Treatment of CKD-MBD in children requires special consideration in order to maximize growth, optimize skeletal health, and prevent cardiovascular disease.

Keywords: CKD-mineral and bone disorder; Children; Chronic kidney disease; Pathogenesis; Treatment of CKD-MBD.

Publication types

  • Review

MeSH terms

  • Calcinosis / prevention & control*
  • Cardiovascular Diseases / prevention & control*
  • Child
  • Chronic Kidney Disease-Mineral and Bone Disorder / therapy*
  • Fibroblast Growth Factor-23
  • Fractures, Bone / prevention & control*
  • Humans
  • Hyperparathyroidism, Secondary / drug therapy*
  • Hyperphosphatemia / therapy*
  • Phosphorus, Dietary

Substances

  • FGF23 protein, human
  • Phosphorus, Dietary
  • Fibroblast Growth Factor-23