TY - CHAP
T1 - Bone loss in chronic kidney disease
AU - Lu, Kuo Cheng
AU - Zheng, Cai Mei
AU - Wu, Chia Chao
AU - Chu, Pauling
PY - 2012/12
Y1 - 2012/12
N2 - Patients with chronic kidney disease (CKD) often develop "chronic kidney disease-mineral and bone disorder" (CKD-MBD). This systemic CKD-related syndrome is manifested by complex abnormalities in bone and mineral metabolism-including bone lesions referred to as renal osteodystrophy (ROD)-and/or extraskeletal calcification. Disruptions in mineral metabolism and bone microarchitecture occur early in the course of CKD, typically beginning as a high bone turnover rate resulting from secondary hyperparathyroidism (SHPT). The condition worsens with the progressive decline in kidney function, as the high bone turnover leads to reduced bone mineral density (BMD) during the course of chronic renal failure. Patients with SHPT exhibit preferential loss of cortical bone (e.g., the distal radius and the femoral neck), often with preserved or slightly increased cancellous bone (e.g., the lumbar spine). Several factors impact the progression of CKD-MBD. In CKD stages 3 and 4, patients with diabetes have lower cortical bone BMD when compared with non-diabetic patients. Calcium load also has a negative impact on the progression of vascular calcification in dialysis patients with adynamic bone disease. Low bone volume is associated with increased coronary calcifications in patients on dialysis, with the degree of risk dependent on the patient's age and dialysis duration. Regular treatments with heparin or anti-platelet drugs also impact BMD in hemodialysis (HD) patients. Low BMD is a major risk factor for hip fracture, and this risk is exacerbated in patients undergoing peritoneal dialysis (PD), who show a significant reduction in cortical BMD. Following kidney transplantation, the greatest rates of bone loss and increased fracture rates are observed in the first 6-18 months, caused by both pre-transplantation bone disease and immunosuppressive therapy. Various medical treatments for SHPT can improve bone mass. Patients with refractory SHPT may require a parathyroidectomy (PTX), which provides marked, sustained improvements in BMD. Markers of bone turnover can predict how PTX will change BMD. Renal osteodystrophy can't be assessed by BMD measurements alone; the gold standard for ROD diagnosis is based on histomorphological changes revealed by bone biopsy. However, because of technical difficulties and a lack of testing facilities, it is often more convenient to use several serum bone markers to measure changes in bone turnover. The combined use of BMD and marker measurements may be a valuable approach in clinical practice.
AB - Patients with chronic kidney disease (CKD) often develop "chronic kidney disease-mineral and bone disorder" (CKD-MBD). This systemic CKD-related syndrome is manifested by complex abnormalities in bone and mineral metabolism-including bone lesions referred to as renal osteodystrophy (ROD)-and/or extraskeletal calcification. Disruptions in mineral metabolism and bone microarchitecture occur early in the course of CKD, typically beginning as a high bone turnover rate resulting from secondary hyperparathyroidism (SHPT). The condition worsens with the progressive decline in kidney function, as the high bone turnover leads to reduced bone mineral density (BMD) during the course of chronic renal failure. Patients with SHPT exhibit preferential loss of cortical bone (e.g., the distal radius and the femoral neck), often with preserved or slightly increased cancellous bone (e.g., the lumbar spine). Several factors impact the progression of CKD-MBD. In CKD stages 3 and 4, patients with diabetes have lower cortical bone BMD when compared with non-diabetic patients. Calcium load also has a negative impact on the progression of vascular calcification in dialysis patients with adynamic bone disease. Low bone volume is associated with increased coronary calcifications in patients on dialysis, with the degree of risk dependent on the patient's age and dialysis duration. Regular treatments with heparin or anti-platelet drugs also impact BMD in hemodialysis (HD) patients. Low BMD is a major risk factor for hip fracture, and this risk is exacerbated in patients undergoing peritoneal dialysis (PD), who show a significant reduction in cortical BMD. Following kidney transplantation, the greatest rates of bone loss and increased fracture rates are observed in the first 6-18 months, caused by both pre-transplantation bone disease and immunosuppressive therapy. Various medical treatments for SHPT can improve bone mass. Patients with refractory SHPT may require a parathyroidectomy (PTX), which provides marked, sustained improvements in BMD. Markers of bone turnover can predict how PTX will change BMD. Renal osteodystrophy can't be assessed by BMD measurements alone; the gold standard for ROD diagnosis is based on histomorphological changes revealed by bone biopsy. However, because of technical difficulties and a lack of testing facilities, it is often more convenient to use several serum bone markers to measure changes in bone turnover. The combined use of BMD and marker measurements may be a valuable approach in clinical practice.
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M3 - Chapter
AN - SCOPUS:84892002290
SN - 9781624171697
SP - 1
EP - 32
BT - Bone Loss
PB - Nova Science Publishers, Inc.
ER -