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Association between Serum Zinc Levels and Trabecular Bone Scores among Patients Undergoing Chronic Hemodialysis
Mayuko Hori1, Hiroshi Takahashi2, Chika Kondo1
1Department of Nephrology, Masuko Memorial Hospital, Nagoya, Japan.
Introduction:
Zinc, an essential trace element, plays an important role in various cellular processes, and zinc deficiency is common in patients undergoing hemodialysis. Zinc has been shown to stimulate osteoblastic bone formation and mineralization and inhibit osteoclastic bone resorption. Although osteoporosis is highly prevalent among patients undergoing hemodialysis, the utility of areal bone mineral density (aBMD) measured using dual-energy X-ray absorptiometry (DXA) is limited because DXA cannot reveal bone microarchitectural alterations. The trabecular bone score (TBS) extracted from DXA images is a new texture measurement used to assess the bone microarchitecture. However, whether zinc status is associated with TBS in patients undergoing hemodialysis remains unclear. Therefore, we investigated the association between serum zinc levels and osteoporosis parameters (aBMD and TBS) in patients undergoing chronic hemodialysis.
Methods:
This cross-sectional study included 316 outpatients undergoing hemodialysis at the Masuko Memorial Hospital in Japan. Serum zinc levels were measured, and aBMD and TBS were assessed using DXA.
Results:
In total, 139 (41.0%) patients had zinc deficiency, defined as serum zinc levels <60 µg/dL. In multivariate linear regression analyses, high serum zinc levels were associated with high TBS (β = 0.146, p = 0.004) but not aBMD values (total hip aBMD: β = -0.0200, p = 0.63; lumbar spine aBMD: β = 0.0478, p = 0.34). In multiple logistic regression analysis, zinc deficiency was associated with degraded bone microarchitecture according to the TBS (odds ratio, 2.27; 95% confidence interval, 1.22-4.22; p = 0.009). No association was found between the serum zinc status and aBMD thresholds for osteoporosis.
Conclusion:
These results suggest that zinc plays a protective role in bone metabolism by inhibiting chronic kidney disease-induced changes in the bone microarchitecture.
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