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Review
. 2008 Feb;23(2):195-207.
doi: 10.1007/s00467-007-0671-3. Epub 2007 Nov 28.

Chronic kidney disease mineral and bone disorder in children

Katherine Wesseling  1 , Sevcan Bakkaloglu, Isidro Salusky
Affiliations
Review

Chronic kidney disease mineral and bone disorder in children

Katherine Wesseling et al. Pediatr Nephrol. 2008 Feb.

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. Decreased activity of renal 1 alpha hydroxylase results in decreased intestinal calcium absorption, increased serum parathyroid hormone levels, and high-turnover renal osteodystrophy, with subsequent growth failure. Simultaneously, phosphorus retention exacerbates secondary hyperparathyroidism, and elevated levels contribute to cardiovascular disease. Treatment of hyperphosphatemia and secondary hyperparathyroidism improves growth and high-turnover bone disease. However, target ranges for serum calcium, phosphorus, and parathyroid hormone (PTH) levels vary according to stage of CKD. Since over-treatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardiovascular calcifications, therapy must be carefully adjusted to maintain optimal serum biochemical parameters according to stage of CKD. Newer therapeutic agents, including calcium-free phosphate binding agents and new vitamin D analogues, effectively suppress serum PTH levels while limiting intestinal calcium absorption and may provide future therapeutic alternatives for children with CKD.

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Figures

Fig. 1
Fig. 1
Schematic representation of the interplay between PTH, FGF-23, and calcitriol in mineral metabolism in vivo. Solid arrows represent the actions of PTH, while open arrows represent those of FGF-23
See this image and copyright information in PMC

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