Therapeutic management becomes increasingly complex in advanced CKD, where fracture risk is high, and evidence for osteoporosis treatments is limited, and evidence for osteoporosis treatments is limited.
Abstract
Chronic kidney disease-mineral and bone disorder is a major contributor to skeletal fragility in patients with chronic kidney disease and after kidney transplantation. Alterations in mineral metabolism begin early during CKD and persist through later stages, leading to a markedly increased fracture risk that may precede renal failure. Bone fragility in CKD arises from the interplay of primary osteoporosis, secondary causes, and CKD-specific disturbances in bone turnover and mineralisation. CKD related bone disease and post-transplant bone loss are characterised not only by reduced bone mineral density but also by impaired bone quality, driven by abnormalities in trabecular and cortical microarchitecture, collagen properties, and mineral composition. Immunosuppressive therapy further exacerbates skeletal vulnerability after kidney transplantation. Recent guidelines have therefore adopted the term CKD-associated osteoporosis to emphasise the need for integrated diagnostic and therapeutic approaches. Diagnosis remains challenging because BMD alone fails to capture alterations in bone turnover and mineralisation that critically influence fracture risk and treatment response. Although bone biopsy remains the reference standard, limited availability has led to increased reliance on bone turnover markers, particularly those not cleared by the kidneys. Combined assessment of parathyroid hormone and BTMs improves discrimination of turnover states and supports individualised clinical decision-making. A pragmatic approach could be based on an integrated evaluation of CKD-MBD parameters, BTM trends, and baseline and follow-up imaging. Therapeutic management becomes increasingly complex in advanced CKD, where fracture risk is high, and evidence for osteoporosis treatments is limited. Antiresorptive, osteoanabolic, and dual-action agents have distinct effects on bone modelling and remodelling, with important implications for efficacy and safety. Despite progress, no consensus exists on optimal treatment strategies. Emerging sequential and combination therapies remain insufficiently studied in advanced CKD and transplant populations, underscoring the need for robust clinical evidence.
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.
O. Nishkumay, O. Iaremenko, V.E. Kondratiuk et al.· International Journal of End...· 0 citations
Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) is a multifaceted syndrome marked by disturbances in bone and mineral metabolism due to chronic kidney disease (CKD). These disruptions involve imbalances in calcium, phosphate, vitamin D, and parathyroid hormone (PTH) levels, which can result in skeletal deformities, vascular calcification, and heightened cardiovascular risk. This article explores the connection between CKD-MBD and bone metabolism, emphasizing the dynamic processes of bone formation and resorption influenced by both systemic and local factors. It discusses the pathophysiology of CKD-MBD, including changes in vitamin D metabolism and the development of secondary hyperparathyroidism. Additionally, the article outlines clinical manifestations such as fractures and cardiovascular complications, along with advanced diagnostic tools and treatment strategies. Effective management of CKD-MBD—through phosphate control, vitamin D supplementation, and the use of calcimimetics—is essential for enhancing patient outcomes. By examining the interactions between CKD, mineral metabolism, and bone health, this article highlights the need for comprehensive strategies to mitigate the systemic effects of CKD-MBD.
Itidal Alatawi· Journal of Biological Insigh...· 0 citations
Chronic kidney disease–associated osteoporosis (CKD-OP) is a highly prevalent—yet frequently underrecognized—condition in patients with advanced CKD. The assessment of bone turnover, mineralization, and volume remains challenging in clinical practice, often requiring bone histomorphometric analysis. Using data from the Brazilian Registry of Bone Biopsies (REBRABO), we identified clinical characteristics associated with these histomorphometric parameters. These findings may help clinicians better characterize the underlying bone phenotype and support a more individualized approach to the diagnosis and management of CKD-associated osteoporosis. Chronic kidney disease–associated osteoporosis (CKD-OP) is characterized by impaired bone quality, and management of bone fragility in CKD partially relies on evaluating bone turnover (T), mineralization (M), and volume (V), through bone biopsy. However, bone biopsy data from large population-based cohorts are limited, making it challenging to identify clinical parameters that are associated with TMV patterns. This cross-sectional study is based on data from the Brazilian Registry of Bone Biopsy (REBRABO) and includes 374 iliac crest bone biopsies from adult patients with CKD5D (median age 51 y), collected between August/15 and December/21. Each biopsy was classified according to bone turnover (low/normal vs. high), mineralization (normal vs. abnormal), and trabecular volume (normal vs. low). Demographic and laboratory parameters were also analyzed. No significant differences in TMV classification were observed based on ethnicity, sex, or diabetes status. Higher turnover was independently associated with younger age, hemodialysis modality, elevated parathyroid hormone (PTH), and alkaline phosphatase (ALP) levels, in a model adjusted for dialysis vintage, prior parathyroidectomy (PTX), and phosphate. Abnormal mineralization was independently associated with age, prior PTX, and lower serum calcium and phosphate, after adjustment for body mass index (BMI), PTH, and ALP. Low trabecular volume was independently associated with older age and lower BMI, in a model adjusted for PTH and history of fractures, and cannot be reliably inferred from biochemical markers. Notably, most patients with adynamic bone also presented with low trabecular volume. Our findings suggest that younger patients undergoing hemodialysis with elevated PTH and ALP levels may benefit from a more intensive approach to the management of hyperparathyroidism. In contrast, older and more frail patients with relatively low PTH levels may be more likely to exhibit low bone volume and turnover and could potentially benefit from therapies aimed at stimulating bone formation, such as anabolic agents.
Eduardo J. Duque, Lauren S. Lowe, C. Carbonara et al.· Archives of Osteoporosis· 0 citations
A practical clinical framework is proposed that integrates endocrine phenotype, vertebral imaging, trabecular bone score, and biochemical assessment into fracture-risk stratification and therapeutic decision-making, enabling improved identification of high- and very-high-risk patients and facilitating the appropriate use of anabolic and antiresorptive therapies.
I. Cincione, Robert A. Marcantonio, Marcellino Monda et al.· Frontiers in Endocrinology· 0 citations
Effective care in cases of male osteoporosis requires an integrated risk-based approach that extends beyond BMD to include clinical risk factors, secondary causes, and functional status, and improved recognition and sex-specific management strategies are essential to reduce the fracture burden and improve long-term outcomes in men.
Selin Tekin, Alper Gürlek· Turkish Journal of Medical S...· 0 citations
Fracture risk increases along the progression of chronic kidney disease (CKD) to become several-fold higher in patients with CKD G4-5D as compared to the kidney-healthy background population matched for age and sex. In 2023, Kidney Disease Improving Global Outcomes (KDIGO) introduced the term CKD-associated osteoporosis to acknowledge and emphasize the overlap in diagnostic workup and therapeutic choices when treating bone fragility in CKD versus other conditions of osteoporosis, while maintaining the need to individualise the treatment plan with knowledge of CKD. Although evidence-based practice guidelines promote management strategies that are widely accepted in postmenopausal women and elderly men, there is a clear need to perform randomized controlled trials to confirm or disprove the benefits of therapy in the setting of advanced CKD. Lifestyle modification, as a 'low risk/potentially high return' intervention, should be considered in all patients. Current evidence furthermore supports a sequential approach to treatment, where mineral metabolism should be optimised, including parathyroid hormone targeting therapy, before initiating bone targeting drugs. We review the current standards of treatment and discuss novel developments in the pathophysiology, diagnosis, outcome prediction and management of CKD-associated osteoporosis and propose a pragmatic treatment algorithm, pending more definite evidence from appropriately designed and powered clinical trials.
P. Evenepoel, H. S. Jørgensen· Nephrology, Dialysis and Tra...· 0 citations