Theme |
Up-to-date renal replacement therapy for diabetic nephropathy -- Standardization and personalization |
Title |
Prevention of and treatment for bone disorder complications in dialysis patients with diabetes mellitus |
Author |
Yoshihiro Tsujimoto |
Inoue Hospital |
Author |
Tsutomu Tabata |
Inoue Hospital |
Author |
Hideki Tahara |
Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine |
Author |
Tetsuo Shoji |
Geriatrics and Vascular Medicine, Osaka City University Graduate School of Medicine |
Author |
Masanori Emoto |
Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine |
Author |
Masaaki Inaba |
Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine |
[ Summary ] |
In patients with diabetes mellitus, hyperglycemia, insulin deficiency and advanced glycation endproducts (AGE) suppress parathyroid cell and osteoblastic cell functions. They bring about a decrease in parathyroid hormone secretion and lowered bone turnover. AGE also influences bone collagen and increases the fragility of bones. In consequence, bone quality is impaired. In dialysis patients with diabetes, a higher incidence of bone fractures is reported, caused by deterioration in bone quality independent of bone mineral density. Malnutrition is also associated with bone fractures in dialysis patients. Moreover, bone disorders are closely linked to vascular calcification and cardiovascular complications in chronic kidney disease patients. In diabetic dialysis patients, vascular calcification and cardiovascular disease are also more often seen than in non-diabetic dialysis patients. Vascular calcification may accelerate not only because of hyperphosphatemia or hypercalcemia but also due to poor glycemic control. Therefore, we must be careful with P, Ca, PTH and glycemic control, as well as nutritional states for CKD-MBD management of patients with diabetes mellitus. |