Abstract

Fragility fractures occur in all stages of chronic kidney disease (CKD) due to low bone mineral density and poor bone quality (namely osteoporosis), as well as in CKD-mineral and bone disorders (CKD-MBD). As in postmenopausal women and older adults, the prompt identification of CKD subjects with a history of fragility fractures is crucial in order to implement strategies to reduce the risk of new fragility fractures and their consequences. The treatment of severe osteoporosis for patients with stages 1-3 CKD should not differ from patients without CKD, while clinical decisions and pharmacological treatments in subjects with stages 4-5/5D CKD differ greatly, being more tricky and challenging. Before starting a pharmacological therapy in subjects with stages 4-5/5D CKD and a history of fragility fractures, it is imperative to discriminate between osteoporosis and CKD-MBD, using quantitative bone histomorphometry. After the implementation of general non-pharmacological measures for fractures and falls risk reduction, the management of osteoporotic patients in stages 4-5/5D CKD may consider the use of bisphosphonates and denosumab, though evidence for safety and efficacy is marginal in advanced CKD. Although alendronate, risedronate and denosumab have been shown to be effective (in reducing fracture incidence), safe and well tolerated in stage 4 CKD, further evidence are warranted before suggesting their systematic use in patients with stage 4 CKD. On the other hand, the pharmacological treatment in patients with stage 5/5D CKD has been explored only in small reports/series producing poor or limited evidence. In all cases (stages 4-5/5D), physicians should be aware of the potential risk of adverse events such as the adynamic bone disease or hypocalcaemia.

KEYWORDS: fractures, chronic kidney disease, osteoporosis, bisphosphonate, denosumab