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Evaluation of Bone Biomarkers in Renal Osteodystrophy.

Life (Basel)

November 2024

Division of Nephrology, Hospital Universitário Clementino Fraga Filho, Federal University of Rio de Janeiro, Rua Prof. Rodolpho Paulo Rocco, 255-Cidade Universitária, Rio de Janeiro 21941-617, RJ, Brazil.

Renal osteodystrophy (ROD) represents histological bone changes in patients with chronic kidney disease and is classified according to turnover and mineralization. This cross-sectional study evaluates several bone biomarkers and their ability to discriminate turnover and mineralization defects in hemodialysis (HD) patients. Bone-specific [BSAP] and total [tAP] alkaline phosphatase, procollagen-1 N-terminal propeptide [P1NP], C-terminal cross-linking telopeptide [CTX], intact [iPTH] and whole [wPTH] parathyroid hormone, sclerostin [SOST], fibroblast growth factor 23 [FGF-23], vitamin D, osteoprotegerin [OPG], and receptor activator of nuclear factor κB ligand [RANKL] were collected before the bone biopsy.

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Article Synopsis
  • Uremic leontiasis ossia (ULO) is a rare condition linked to renal osteodystrophy in patients with end-stage chronic kidney disease (CKD) and secondary hyperparathyroidism (SHPTH), causing bone deformities that can lead to a 'leonine' facial appearance.
  • The case study focuses on a 39-year-old female patient undergoing treatment, who exhibited significant symptoms and had elevated parathyroid hormone (PTH) levels, confirmed by CT scans.
  • Treatment involves a multidisciplinary approach including surgery and management of SHPTH to correct anatomical issues and prevent further complications.
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Article Synopsis
  • Leontiasis ossea, or craniofacial fibrous dysplasia, is a rare condition that causes abnormal growth of facial bones, often linked to chronic kidney disease and high parathyroid hormone levels.
  • A case of a 30-year-old male with severe facial swelling and bone changes highlights the rapid progression of symptoms after poor dialysis access and the persistence of hyperparathyroidism despite treatment efforts.
  • The article also reviews the underlying causes, imaging techniques used for diagnosis, and management strategies for this complex disease.
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The Challenge of Fractures in Patients with Chronic Kidney Disease.

Endocr Pract

December 2024

Division of Endocrinology, Diabetes, Metabolism, and Nutrition Mayo Clinic, Rochester, MN.

People with chronic kidney disease (CKD) are at increased risk of fractures in comparison to the non-CKD population and fractures are associated with high mortality and worsening quality of life. The higher risk observed in the CKD population is related to the complex interplay of CKD-mineral bone disorder (MBD) abnormalities causing changes in bone turnover (T), mineralization (M), and volume (V), along with other risk factors accumulated as glomerular filtration rate declines. The approach for evaluation of bone disease and fracture risk in CKD is different from the approach in the general population.

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Clinical Utility of Bone Turnover Markers in Chronic Kidney Disease.

J Bone Metab

November 2024

Division of Clinical Medicine, School of Medicine and Population Health, University of Sheffield, Sheffield, UK.

Chronic kidney disease (CKD) often leads to mineral and bone disorders (CKD-MBDs), which are nearly universal in patients undergoing dialysis. CKD-MBD includes abnormal calcium-phosphate metabolism, vascular and soft tissue calcification, and bone abnormalities (renal osteodystrophy [ROD]). Bone fragility in CKD occurs due to low bone mass and poor bone quality, and patients with CKD have higher fracture and mortality rates.

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