Fragility Fractures in Chronic Kidney Disease: Assessment and Pharmacologic Management

Fractures are common in all stages of chronic kidney disease (CKD), and are associated with increased morbidity and mortality. Both CKD and osteoporosis often coexist as they both are strongly age associated. However, the management of fragility fractures in CKD poses many dilemmas. These include diagnosing the aetiology of fractures and choosing appropriate treatment. This paper reviews the current evidence for the assessment and pharmacologic management of fragility fractures in CKD. 1. Introduction The burden of fracture has been shown to be high in all stages of chronic kidney disease (CKD). Studies have consistently shown that end stage kidney disease (ESKD) and dialysis are risk factors for low trauma fracture independent of age [1]. More recent studies have demonstrated that age adjusted prevalence of fracture is high even in early stages of CKD, including in those with age associated renal impairment [2]. Although the exact mechanisms responsible for the increased fracture risk in CKD have not been fully elucidated, it is not entirely unexpected as disorders of bone remodeling are observed as early as when eGFR is <60？ml/min/1.73？m2 [3]. However, the management of this common problem remains a challenge for many reasons. The diagnosis of the aetiopathology of fractures in CKD is not straightforward as, unlike in the general population, the fractures in CKD can be due to a heterogeneous group of bone disorders besides osteoporosis. Furthermore, the efficacy and safety of current osteoporosis therapies remain speculative in CKD. 2. Diagnosis of Osteoporosis and Fracture Risk Assessment The current methods of diagnosing osteoporosis or predicting fractures either by the presence of a low trauma fracture or on the basis of bone mineral density (BMD) criteria (a T score of 2.5 standard deviations or more below the young adult mean BMD) by dual energy X-ray absorptiometry (DEXA) [4] have not been validated in chronic kidney disease (CKD). Although cross-sectional studies show that both dialysis and predialysis patients [5, 6] with fractures have a lower BMD compared with those without, fracture prediction by BMD has not been validated prospectively in CKD. The biochemical abnormalities of CKD have now been recognized for their pathogenetic role not only in renal bone disease, often described as renal osteodystrophy (ROD), but also in a wide spectrum of disorders including vascular calcification and increased cardiovascular risk. As the definition of ROD does not adequately describe this diverse spectrum of disorders, the term chronic kidney