Pediatr Nephrol (2008) 23:195–207 DOI 10.1007/s00467-007-0671-3 EDUCATIONAL FEATURE Chronic kidney disease mineral and bone disorder in children Katherine Wesseling & Sevcan Bakkaloglu & Isidro Salusky Received: 14 May 2007 / Revised: 15 August 2007 / Accepted: 23 September 2007 / Published online: 28 November 2007 # IPNA 2007 Abstract Childhood and adolescence are crucial times for the development of a healthy skeletal and cardiovascular system. Disordered mineral and bone metabolism accom- pany 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 absorp- tion, increased serum parathyroid hormone levels, and high-turnover renal osteodystrophy, with subsequent growth failure. Simultaneously, phosphorus retention exac- erbates secondary hyperparathyroidism, and elevated levels contribute to cardiovascular disease. Treatment of hyper- phosphatemia and secondary hyperparathyroidism im- proves growth and high-turnover bone disease. However, target ranges for serum calcium, phosphorus, and parathy- roid hormone (PTH) levels vary according to stage of CKD. Since over-treatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardio- vascular calcifications, therapy must be carefully adjusted to maintain optimal serum biochemical parameters accord- ing to stage of CKD. Newer therapeutic agents, including K. Wesseling : I. Salusky Pediatric Nephrology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA S. Bakkaloglu Pediatric Nephrology, Gazi University, Ankara, Turkey K. Wesseling (*) Pediatric Nephrology, UCLA, 2-383 MDCC, 650 Charles Young Drive, Los Angeles, CA 90095, USA e-mail: kwesseling@mednet.ucla.edu 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. Keywords Osteodystrophy . Growth . Vascular calcification . Parathyroid hormone (PTH) . Vitamin D . CKD mineral and bone disorder . Pediatrics Introduction Childhood and adolescence are crucial times for the development of a healthy skeletal and vascular system; alterations in bone modeling/remodeling or vascular biolo- gy in youth carry consequences that severely impact on quality of life as well as life span. In childhood, chronic kidney disease (CKD) causes disordered regulation of mineral metabolism, with subsequent alterations in bone modeling, remodeling, and growth. These alterations occur early in the course of CKD and are accompanied by the development of cardiovascular calcifications. Since growth failure and short stature are clinically apparent and concerning to patients, families, and physicians alike, optimization of growth and final adult height has been a focus of CKD management in children for decades. More recently, however, a growing awareness that cardiovascular calcifications accompany CKD, that cardiovascular disease is the leading cause of mortality in both adults and children with kidney disease, and that therapies designed to treat the skeletal consequences of CKD affect the progression of vascular pathology, has led to a reclassification of the mineral, skeletal, and vascular disease associated with progressive kidney failure. Together, these alterations are termed “CKD mineral and bone disorder” (“CKD-MBD”) [1].