Bone strength is determined not only by bone quantity [bone mineral density (BMD)] but also by bone quality, including matrix composition, collagen fiber arrangement, microarchitecture, geometry, mineralization, and bone turnover, among others. These aspects influence elasticity, the load-bearing and repair capacity of bone, and microcrack propagation and are thus key to fractures and their avoidance. In chronic kidney disease (CKD)-associated osteoporosis, factors traditionally associated with a lower bone mass (advanced age or hypogonadism) often coexist with non-traditional factors specific to CKD (uremic toxins or renal osteodystrophy, among others), which will have an impact on bone quality. The gold standard for measuring BMD is dual-energy X-ray absorptiometry, which is widely accepted in the general population and is also capable of predicting fracture risk in CKD. Nevertheless, a significant number of fractures occur in the absence of densitometric World Health Organization (WHO) criteria for osteoporosis, suggesting that methods that also evaluate bone quality need to be considered in order to achieve a comprehensive assessment of fracture risk. The techniques for measuring bone quality are limited by their high cost or invasive nature, which has prevented their implementation in clinical practice. A bone biopsy, high-resolution peripheral quantitative computed tomography, and impact microindentation are some of the methods established to assess bone quality. Herein, we review the current evidence in the literature with the aim of exploring the factors that affect both bone quality and bone quantity in CKD and describing available techniques to assess them.

Osteoporosis and fragility fractures are among the most prevalent and clinically significant complications in patients with chronic kidney disease (CKD), particularly in stages G4–G5 and in those undergoing dialysis (G5D). These skeletal disorders are associated with markedly increased morbidity and mortality, including a 2- to 9-fold higher risk of hip fractures compared to the general population, prolonged hospitalization, functional decline, and excess postoperative mortality. Despite this substantial burden, CKD-associated osteoporosis remains underrecognized and undertreated. Limited inclusion of CKD patients in pivotal osteoporosis trials and the absence of high-evidence guidance in clinical guidelines have contributed to a persistent therapeutic gap. PTH analog agents such as teriparatide and abaloparatide have demonstrated robust efficacy in increasing bone mass and reducing fracture risk in the general population. However, their use in CKD remains limited. PTH analog are poorly prescribed in patients with CKD stage G3 and remain off-label for stages G4–G5D, despite the high prevalence of adynamic bone disease across all stages of CKD. Abaloparatide, a selective PTH1 receptor agonist, exerts potent anabolic effects with a lower incidence of hypercalcemia than teriparatide and may offer a favourable safety profile in carefully selected patients. Preliminary data suggest preservation of bone microarchitecture and potential benefits in low-turnover bone disease, although evidence in CKD is still limited. This narrative review examines current evidence on abaloparatide’s potential role in CKD, emphasizing its mechanism of action, efficacy, safety, and relevance for patients with low bone turnover and high fracture risk.