Chronic kidney disease (CKD) is associated with increased fracture risk and post-fracture mortality. CKD-associated osteoporosis arises from the combined effects of traditional pathways (e.g., age-related bone loss) and CKD-specific mechanisms (e.g., disturbances in mineral metabolism) that contribute to bone fragility. Dual-energy X-ray absorptiometry (DXA), serum calcium, phosphorus, 25-hydroxyvitamin D, parathyroid hormone (PTH), and bone turnover markers that are not cleared by the kidneys are used to assess bone health in patients with CKD. Bone biopsy may be used to directly assess bone turnover, mineralization and volume to guide treatment in patients with advanced CKD. Antiresorptive and anabolic therapies for osteoporosis have demonstrated efficacy and safety in mild to moderate stages of CKD, but there are limited data to guide the use of these drugs in CKD stages 4-5. Oral bisphosphonates and denosumab may be effective in advanced CKD, but no study to date has demonstrated a fracture risk reduction in this group. Hypocalcemia and other safety concerns limit the use of denosumab in patients with advanced CKD. PTH analogues and romosozumab demonstrate improvements in bone mineral density in CKD stages 4-5, but more data is needed to support the use of these drugs in this population.
Mulroy et al. (Tue,) studied this question.