A structural approach to skeletal fragility in chronic kidney disease.

Renal osteodystrophy is a multifactorial disorder of bone metabolism in chronic kidney disease (CKD). As CKD progresses, ensuing abnormalities in mineral metabolism result in distortions in trabecular microarchitecture, thinning of the cortical shell, and increased cortical porosity. Recent studies have shown significantly increased hip fracture rates in CKD stages 3 and 4, in dialysis patients, and in transplant recipients. The majority of studies of bone loss in CKD relied on dual-energy x-ray absorptiometry (DXA) measures of bone mineral density. However, DXA summarizes the total bone mass within the projected bone area, concealing distinct structural alterations in trabecular and cortical bone. Recent data have confirmed that peripheral quantitative computed tomography (pQCT) measures of cortical density and thickness provide substantially better fracture discrimination in dialysis patients, compared with hip or spine DXA. This review summarizes the growing evidence for bone fragility in CKD stages 3 through 5, considers the effects of CKD on trabecular and cortical bone structure as it relates to fracture risk, and details the potential advantages and disadvantages of DXA and alternative measures of bone density, geometry, and microarchitecture, including pQCT, high-resolution pQCT, and micro-magnetic resonance imaging for fracture risk assessment in CKD.