Uremic osteoporosis
Junichiro J Kazama1, Yoshiko Iwasaki2, Masafumi Fukagawa3
1Division of Blood Purification Therapy, Niigata University Medical and Dental Hospital , Niigata, Japan.
Insights
Chronic kidney disease (CKD) patients face a high hip fracture risk due to factors beyond falls. New research suggests
Area of Science:
- Nephrology and Orthopedics
- Bone Biology and Disease
Background:
- Chronic kidney disease-related mineral and bone disorder (CKD-MBD) involves bone abnormalities, but hip fracture risk in CKD patients is complex.
- While falls contribute, other mechanisms are involved in the elevated hip fracture risk observed in CKD populations.
- The relationship between bone mineral density and fracture risk differs in CKD patients compared to the general population.
Approach:
- Investigated the mechanical properties of long bones in experimental CKD animal models.
- Examined the correlation between bone elasticity, bone biochemical changes, and kidney function.
- Assessed the effect of the oral absorbent AST-120 on bone material properties and elasticity in CKD animals.
Key Points:
- Bone elasticity in CKD animals inversely correlated with kidney function, indicating impaired bone material properties.
- Deterioration of bone elasticity was significantly linked to bone biochemical alterations.
- AST-120 administration prevented the decline in bone elasticity and material properties.
Conclusions:
- Uremic toxins appear to degrade bone material properties, leading to reduced bone elasticity.
- This 'uremic osteoporosis' is distinct from CKD-MBD and may be a primary driver of increased hip fracture risk in CKD patients.
- Understanding uremic osteoporosis offers new insights into managing fracture risk in CKD.
Abstract:
Abnormalities in bone turnover, mineralization, and volume represent one of the three components of chronic kidney disease-related mineral and bone disorder (CKD-MBD). The risk of hip fracture is considerably high, while the risk of spinal compression fracture may not be more elevated among CKD patients than in general population. The relationship between bone fracture and bone mineral density in CKD patients is more complex than in those without kidney disease. An increase in the rate of falls has been reported to be a major cause of high hip fracture risk among CKD patients; however, it certainly is not the only underlying mechanism. Abnormal parathyroid function is not likely to be a major cause of hip fracture among CKD patients. In experimental CKD animals, mechanical elasticity properties of long bones showed an inverse correlation with kidney function. The deterioration of bone elasticity showed a significant correlation with bone biochemical changes. Of note, administration of the oral absorbent AST-120 was capable of preventing both changes. These findings suggest that uremic toxins cause a deterioration of bone material properties, and changes in material properties disturb bone elasticity. This disease concept cannot be considered to be a direct consequence of CKD-MBD. We therefore would like to call it 'uremic osteoporosis'. This entity may be a major cause of increased hip fracture risk among CKD patients.
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