Abstract
Children with long-standing chronic kidney disease (CKD) display clinical symptoms of bone disease, including bony deformities and fractures, which contribute to long-standing disability. Abnormalities in skeletal mineralization occur in a substantial proportion of this population and may contribute to chronic morbidity. Underscoring the potential contribution of parameters other than bone turnover to bone disease in CKD, a new definition for renal osteodystrophy (ROD), emphasizing the assessment of three key histologic descriptors, i.e., bone turnover (T), mineralization (M), and volume (V) (TMV), has been recommended in the assessment of all patients with CKD. Although bone biopsy is the only available method for assessing all three recommended areas of bone histology, this invasive procedure is not routinely used in any clinical setting; thus, a true understanding of the prevalence of abnormal turnover, defective mineralization, and altered bone volume throughout the course of CKD is limited. Recent data, however, have shed light on the progression of renal ROD throughout the course of CKD, including its early stages, as well as on the alterations in cell biology that accompany ROD.