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Review
. 2013 Mar;33(2):169-79.
doi: 10.1016/j.semnephrol.2012.12.017.

Chronic kidney disease: mineral and bone disorder in children

Katherine Wesseling-Perry  1 , Isidro B Salusky
Affiliations
Review

Chronic kidney disease: mineral and bone disorder in children

Katherine Wesseling-Perry et al. Semin Nephrol. 2013 Mar.

Abstract

Childhood and adolescence are crucial times for the development of a healthy skeletal and cardiovascular system. Disordered mineral and bone metabolism accompany chronic kidney disease (CKD) and present significant obstacles to optimal bone strength, final adult height, and cardiovascular health. Early increases in bone and plasma fibroblast growth factor 23 (FGF23) are associated with early defects in skeletal mineralization. Later in the course of CKD, secondary hyperparathyroidism--caused by a combination of declining calcitriol values and phosphate retention--results in high-turnover renal osteodystrophy whereas increased levels of both phosphate and FGF23 contribute to cardiovascular disease. Treatment of hyperphosphatemia and secondary hyperparathyroidism improves high-turnover bone disease but fails to correct defects in skeletal mineralization. Because overtreatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardiovascular calcifications, therapy therefore must be titrated carefully to maintain optimal serum biochemical parameters according to stage of CKD. Newer therapeutic agents and new treatment paradigms may suppress serum PTH levels effectively while limiting intestinal calcium absorption and skeletal FGF23 stimulation and may provide future therapeutic alternatives for children with CKD.

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Figures

Figure 1
Figure 1
Percentage of pediatric patients with abnormalities in bone turnover (solid) and skeletal mineralization (open) and in circulating PTH (striped) and FGF23 (polka dot) values according to CKD stage.
Figure 2
Figure 2
a. Skeletal expression of FGF23 in normal control (A) and in a patient with early CKD (B). Skeletal expression of DMP1 in normal control (C) and early CKD (D). b. Skeletal expression of FGF23 and DMP1 are increased in all stages of CKD relative to control.
Figure 2
Figure 2
a. Skeletal expression of FGF23 in normal control (A) and in a patient with early CKD (B). Skeletal expression of DMP1 in normal control (C) and early CKD (D). b. Skeletal expression of FGF23 and DMP1 are increased in all stages of CKD relative to control.
See this image and copyright information in PMC

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