Endocrine and metabolic determinants of CKD-associated osteoporosis: diagnostic insights and clinical implications

Abstract

Osteoporosis is defined as a systemic skeletal disorder characterized by decreased bone mineral density (BMD) and deterioration of bone microarchitecture, leading to increased fracture risk. Among the causes of secondary osteoporosis, chronic kidney disease (CKD) plays a crucial role, as the kidneys are central regulators of endocrine mineral metabolism, including calcium, phosphate, vitamin D, and parathyroid hormone, as well as Klotho-FGF23 axis. These disturbances contribute to the deterioration of BMD and bone quality. Collectively, these factors highlight the need to recognize and further define CKD-associated osteoporosis as a distinct clinical entity. While not routinely required, bone biopsy continues to play an important role in selected complex cases where diagnostic uncertainty persists. Among the available markers, bone-specific alkaline phosphatase and tartrate-resistant acid phosphatase 5b are not significantly affected by renal clearance and are therefore considered reliable indicators of bone metabolism in CKD. Additionally, intact N-terminal telopeptide of type I collagen may also be applied in this clinical setting. Presents of calcification in CKD require the new approaches for BMD assessment in kidney impairment. Results indicate that radiofrequency echographic multispectrometry provides BMD and fracture risk assessment comparable to DXA in patients on peritoneal dialysis, while also highlighting the impact of vascular calcifications on the diagnostic accuracy of lumbar spine DXA measurements. Patients with CKD typically have impaired bone microarchitecture, as evidenced by lower trabecular bone score. A comprehensive and collaborative approach is essential to improve diagnostic accuracy and to develop more precise and effective therapeutic strategies for this patient population.