| Theme | How Can We Realize the Philosophy of Chronic Kidney Disease-Mineral and Bone Disorder? | |
|---|---|---|
| Title | Reconsideration of adynamic bone disease mechanisms and treatment | |
| Publish Date | 2010/01 | |
| Author | Masahide Mizobuchi | Division of Nephrology, Department of Medicine, Showa University School of Medicine |
| Author | Yoshihiro Kuno | Division of Nephrology, Department of Medicine, Showa University School of Medicine |
| Author | Tadao Akizawa | Division of Nephrology, Department of Medicine, Showa University School of Medicine |
| [ Summary ] | Renal osteodystrophy (ROD) is a bone morphologic change which occurs in patients with chronic kidney disease (CKD). ROD compromises a wide spectrum of manifestations including high-turnover bone diseases, such as osteitis fibrosa and mixed uremic osteodystrophy, as well as low-turnover bone diseases, such as osteomalacia or adynamic bone disease. The prevalence of adynamic bone disease, which is defined by the presence of low or non―existent bone formation, along with the defects in active osteoblasts and osteoclasts, reportedly increases. Adynamic bone disease in patients with CKD is a clinical concern because of the potential for increased risk for fractures and cardiovascular disease which are associated with mortality in these patients. Important mechanisms by which bone formation is impared are vitamin D receptor―dependent and PTH-receptor dependent pathways. Although multiple circulating factors may interfere with these pathways, the precise mechanisms still remain to be investigated. Further studies are needed to clarify the mechanisms of adynamic bone disease, and the clinical outcomes for patients with this disease. | |