Abstract
Children with chronic kidney disease (CKD) have multiple risk factors for impaired accretion of trabecular and cortical bone. CKD during childhood poses an immediate fracture risk and compromises adult bone mass, resulting in significantly greater skeletal fragility throughout life. High-turnover disease initially results in thickened trabeculae, with greater bone volume. As disease progresses, resorption cavities dissect trabeculae, connectivity degrades, and bone volume decreases. Increased bone turnover also results in increased cortical porosity and decreased cortical thickness. Dual-energy X-ray absorptiometry (DXA)-based measures of bone mineral density (BMD) are derived from the total bone mass within the projected bone area (g/cm2), concealing distinct disease effects in trabecular and cortical bone. In contrast, peripheral quantitative computed tomography (pQCT) estimates volumetric BMD (vBMD, g/cm3), distinguishes between cortical and trabecular bone, and provides accurate estimates of cortical dimensions. Recent data have confirmed that pQCT measures of cortical vBMD and thickness provide substantially greater fracture discrimination in adult dialysis patients compared with hip or spine DXA. The following review considers the structural effects of renal osteodystrophy as it relates to fracture risk and the potential advantages and disadvantages of DXA and alternative measures of bone density, geometry, and microarchitecture, such as pQCT, micro-CT (μCT), and micro magnetic resonance imaging (μMRI) for fracture risk assessment.
Highlights
Renal osteodystrophy is a multifactorial and universal disorder of bone metabolism in chronic kidney disease (CKD)
Link et al reported that transplant recipients had significantly lower MRI measures of BV/TV, Tb.Sp, Tb.Th, and Tb.N compared with controls; [67] spine quantitative CT (QCT), trabecular bone mineral density (BMD), and Dual-energy X-ray absorptiometry (DXA) hip and spine BMD did not differ between transplant recipients and controls
The 2003 National Kidney Foundation Clinical Practice Guidelines for Bone Metabolism and Disease in CKD recommended the following for all adult patients with CKD: [68] “Bone mineral density should be measured by dual energy X-ray absorptiometry in patients with fractures and in those with known risk factors for osteoporosis.”
Summary
Renal osteodystrophy is a multifactorial and universal disorder of bone metabolism in chronic kidney disease (CKD). Children with CKD have multiple risk factors for impaired bone development, including abnormal mineral metabolism, secondary hyperparathyroidism, poor linear growth, delayed. Pediatr Nephrol (2007) 22:1815–1824 development, malnutrition (including vitamin D insufficiency), decreased weight-bearing activity, and immunosuppressive therapies The impact of these threats to bone health may be immediate, resulting in fragility fractures, or delayed, due to suboptimal peak bone mass accrual. The effects of abnormal bone and mineral metabolism on endochondral ossification during growth result in complications in the epiphyseal region that are unique to children with CKD. These complications include linear growth failure, slipped epiphyses, and skeletal deformities resembling vitamin-D-deficient rickets. The following review considers the structural effects of renal osteodystrophy as it relates to fracture risk and the potential advantages and disadvantages of DXA and alternative measures of bone density, geometry, and microarchitecture, such as peripheral quantitative computed tomography (pQCT), micro-CT (μCT), and micro magnetic resonance imaging (μMRI) for fracture risk assessment
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