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

Treatment of Pediatric Chronic Kidney Disease-Mineral and Bone Disorder

Affiliations
Review

Treatment of Pediatric Chronic Kidney Disease-Mineral and Bone Disorder

Mark R Hanudel et al. Curr Osteoporos Rep. 2017 Jun.

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.

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Figures

Figure 1
Figure 1
In pediatric chronic kidney disease (CKD) patients, elevated fibroblast growth factor 23 (FGF23) levels are observed very early in the CKD course (Fig. 1A; 17) and are associated with CKD progression (defined as either dialysis initiation, kidney transplantation, or a 50% reduction in glomerular filtration rate (GFR) from baseline) (Fig. 1B; 57). The association between higher FGF23 levels and CKD progression persists after multivariable adjustment for baseline GFR, proteinuria, blood pressure, glomerular vs. non-glomerular disease, and medication use (angiotensin converting enzyme inhibitors/angiotensin-receptor blockers, vitamin D analogs, and phosphate binders) (57). Used with permission from the American Society of Nephrology.

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