Rational and Objectives
Low intensity vibration (LIV) may represent a nondrug strategy to mitigate bone deficits in patients with end-stage renal disease.
Materials and Methods
Thirty end-stage renal patients on maintenance hemodialysis were randomized to stand for 20 minutes each day on either an active or placebo LIV device. Analysis at baseline and completion of 6-month intervention included magnetic resonance imaging (tibia and fibula stiffness; trabecular thickness, number, separation, bone volume fraction, plate-to-rod ratio; and cortical bone porosity), dual-energy X-ray absorptiometry (hip and spine bone mineral density [BMD]), and peripheral quantitative computed tomography (tibia trabecular and cortical BMD; calf muscle cross-sectional area).
Results
Intention-to-treat analysis did not show any significant changes in outcomes associated with LIV. Subjects using the active device and with greater than the median adherence (70%) demonstrated an increase in distal tibia stiffness (5.3%), trabecular number (1.7%), BMD (2.3%), and plate-to-rod ratio (6.5%), and a decrease in trabecular separation (−1.8%). Changes in calf muscle cross-sectional area were associated with changes in distal tibia stiffness (R = 0.85), trabecular bone volume/total volume (R = 0.91), number (R = 0.92), and separation (R = −0.94) in the active group but not in the placebo group. Baseline parathyroid hormone levels were positively associated with increased cortical bone porosity over the 6-month study period in the placebo group (R = 0.55) but not in the active group (R = 0.01). No changes were observed in the nondistal tibia locations for either group except a decrease in hip BMD in the placebo group (−1.7%).
Conclusion
Outcomes and adherence thresholds identified from this pilot study could guide future longitudinal studies involving vibration therapy.
Introduction
Renal osteodystrophy is a multifactorial and pervasive disorder of bone and mineral metabolism that parallels chronic kidney disease. This pernicious disease reduces bone quantity, disrupts bone turnover, and compromises mineralization processes, resulting in a skeleton highly susceptible to fracture . This higher susceptibility to fracture is based on several factors. For one, elevated expression of the hormone fibroblast growth factor 23 in osteocytes during the early course of chronic kidney disease plays a critical role in the progression of abnormal mineral ion homeostasis by decreasing 1,25(OH) 2 vitamin D and ultimately impairing intestinal calcium absorption and increasing serum parathyroid hormone (PTH) . The overall relative risk for hip fracture has been estimated to be about 4.4 times greater for patients on dialysis as compared to people of the same sex in the general population, and mortality risk following fractures are markedly greater in end-stage renal disease patients compared to healthy adults .
The clinical effectiveness of osteoporosis therapies, such as phosphate binders, calcium, vitamin D, and conventional antiresorptive drugs to prevent fractures in end-stage renal disease has not been well established . To avoid adding yet another drug to their daily intake, it would be useful to improve the bone health of these patients by nonpharmacologic means. Recent studies have suggested that whole-body vibration may have a therapeutic role to play in improving bone health, particularly for individuals who are unable to tolerate exercise . In a 1-year study of adult female sheep, a 20-minute exposure each day to 30 Hz and 0.3g (where g = Earth’s gravitational acceleration, or 9.8m/s 2 ) stimulation resulted in a 30% increase in trabecular bone mineral density (BMD) of the distal femur . In a follow-up study, finite element modeling was used to show that the anabolic response yields reduction in apparent strain magnitude in the trabeculae as well as produces a structure that is stiffer and less prone to fracture for a given load .
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Materials and Methods
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Randomization
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Intervention
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Outcome Measures
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MRI Acquisition
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MRI-based Analysis
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DXA
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pQCT
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Outcome Analyses
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Statistical Analysis
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Results
Participant Characteristics
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Table 1
Characteristics of Participants Randomized to Active or Placebo Device Use
Active
N = 14 Placebo
N = 15 Mean Age (SD), yr 50 (11) 48 (10) Sex, n (%) Male 8 (57) 9 (60) Female 6 (43) 6 (40) Mean body mass (SD), kg 72.7 (18.7) 69.7 (16.4) Mean height (SD), m 1.69 (0.092) 1.68 (0.070) Mean body-mass index (SD), kg/m 2 25.3 (5.33) 24.4 (4.36) Cause of renal disease, n (%) Hypertension 6 (43) 6 (40) Diabetes 1 (7) 1 (7) Focal segmental glomerulosclerosis 4 (29) 2 (13) Other 3 (21) 6 (40) Median dialysis duration [range], yr 2.13 [0.172–15.2] 3.52 [0.339–7.12] Median intentional exercise [range], min/day 25 [0–100] 39 [0–90] Medication intake, n Prednisone 2 2 Cinacalcet 7 3 Vitamin D sterol 15 13 Phosphate binder 14 14
SD, standard deviation.
None of the parameters were significantly different between the two groups.
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Adherence to Daily Device Use
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Intention-to-Treat and Post Hoc Analyses
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Table 2
Percent Changes Between the Two Time Points for the Outcomes (Reported as Mean ± SD), Based on the Intention-to-Treat Data Analysis
Active % Change Placebo % Change_P_ Tibia stiffness, GPa 2.43 ± 5.15 1.61 ± 6.90 .72 Tibia trabecular BV/TV, % 0.30 ± 3.82 −1.21 ± 5.77 .42 Tibia trabecular thickness, mm −0.02 ± 1.32 0.29 ± 1.83 .70 Tibia trabecular number 0.30 ± 2.85 −1.53 ± 4.85 .23 Tibia trabecular separation, mm −0.24 ± 3.31 1.97 ± 5.59 .22 Tibia trabecular plate-to-rod ratio 3.59 ± 8.59 1.26 ± 10.2 .52 Tibia trabecular BMD, mg/cm 3 0.95 ± 2.68 −0.68 ± 3.64 .21 Tibia cortical porosity, % 2.26 ± 13.0 1.63 ± 11.8 .89 Tibia cortical BMD, mg/cm 3 −0.26 ± 1.25 −0.04 ± 0.57 .58 Hip BMD, mg/cm 2 −1.27 ± 3.48 −1.17 ± 2.48 .93 Lumbar PA spine BMD, mg/cm 2 −1.09 ± 2.25 −1.34 ± 4.21 .85 Calf muscle CSA, cm 2 −1.72 ± 3.47 −0.40 ± 6.72 .58 PTH, pg/mL 51.0 ± 134 104 ± 340 .60
BMD, bone mineral density; BV/TV, bone volume/total volume; CSA, cross-sectional area; PA, posteroanterior; PTH, parathyroid hormone; SD, standard deviation.
The P value indicates the significance of the difference in percent change in parameters between the active and placebo groups.
Table 3
Baseline, 6-Month Absolute Values, and Percent Changes Between the Two Time Points for the Outcomes (Reported as Mean ± SD), Based on the Post Hoc Longitudinal Data Analysis
Baseline 6 Months % Change_P_ Tibia stiffness, GPa Active 1.11 ± 0.09 1.17 ± 0.11 5.26 ± 4.5 .022 \* Placebo 1.20 ± 0.17 1.21 ± 0.18 0.94 ± 6.1 .49 Tibia trabecular BV/TV, % Active 8.98 ± 0.06 9.15 ± 0.60 1.87 ± 2.3 .078 Placebo 9.69 ± 1.53 9.56 ± 1.56 −1.23 ± 5.3 .30 Tibia trabecular thickness, mm Active 0.104 ± 0.004 0.104 ± 0.004 0.16 ± 1.2 .75 Placebo 0.108 ± 0.014 0.109 ± 0.012 0.12 ± 1.7 .73 Tibia trabecular number Active 0.862 ± 0.04 0.877 ± 0.05 1.70 ± 1.40 .018 \* Placebo 0.893 ± 0.095 0.880 ± 0.096 −1.39 ± 4.32 .16 Tibia trabecular separation, mm Active 1.06 ± 0.05 1.04 ± 0.06 −1.84 ± 1.55 .020 \* Placebo 1.03 ± 0.13 1.04 ± 0.14 1.76 ± 5.00 .12 Tibia trabecular plate-to-rod ratio Active 1.33 ± 0.27 1.36 ± 0.28 6.51 ± 3.8 .004 \* Placebo 1.27 ± 0.30 1.31 ± 0.31 1.06 ± 10 .64 Tibia trabecular BMD, mg/cm 3 Active 202 ± 32 207 ± 30 2.34 ± 2.3 .034 \* Placebo 216 ± 58 217 ± 49 −0.76 ± 3.3 .31 Tibia cortical porosity, % Active 39.5 ± 7.0 39.5 ± 5.6 −1.64 ± 11 .71 Placebo 37.9 ± 8.3 38.5 ± 6.3 3.07 ± 13 .27 Tibia cortical BMD, mg/cm 3 Active 1135 ± 46.2 1137 ± 43 0.13 ± 0.42 .45 Placebo 1159 ± 45.3 1150 ± 50 −0.25 ± 1.08 .33 Hip BMD, mg/cm 2 Active 1.00 ± 0.19 1.00 ± 0.19 0.14 ± 4.1 .93 Placebo 0.98 ± 0.20 0.91 ± 0.20 −1.65 ± 2.7 .0049 \* Lumbar PA Spine BMD, mg/cm 2 Active 1.06 ± 0.11 1.05 ± 0.11 −0.92 ± 2.3 .32 Placebo 1.05 ± 0.22 1.03 ± 0.23 −1.32 ± 3.7 .11 Calf muscle CSA, cm 2 Active 67.4 ± 13.0 67.1 ± 12.3 −0.34 ± 2.4 .77 Placebo 60.0 ± 13.9 60.2 ± 14.0 −1.08 ± 6.2 .44 PTH, pg/mL Active 333 ± 222 399 ± 238 34 ± 69 .24 Placebo 373 ± 316 352 ± 306 94 ± 299 .18
BMD, bone mineral density; BV/TV, bone volume/total volume; CSA, cross-sectional area; PA, posteroanterior; PTH, parathyroid hormone; SD, standard deviation.
Participants who complied more than the median adherence (70%) in the active mechanical stimulation arm were considered “active” and all other participants are grouped as “placebo.” The P value indicates the significance of the percent change in parameters between the two time points within each group.
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Table 4
Correlation Between the 6-Month Changes in Measured Parameters and Daily Device Adherence in the Active Group Using Post Hoc Analysis
Change (%) vs Adherence R_P_ Tibia stiffness 0.66 .050 \* Tibia trabecular BV/TV 0.87 .0021 \* Tibia trabecular thickness 0.80 .0095 \* Tibia trabecular number 0.75 .021 \* Tibia trabecular separation −0.77 .016 \* Tibia trabecular plate-to-rod ratio 0.75 .020 \* Tibia trabecular BMD 0.60 .11 Tibia cortical porosity −0.86 .0028 \* Tibia cortical density −0.15 .72 Hip BMD 0.14 .72 Lumbar spine BMD −0.29 .44 Calf muscle CSA 0.70 .12 PTH 0.41 .28
BMD, bone mineral density; BV/TV, bone volume/total volume; CSA, cross-sectional area; PTH, parathyroid hormone.
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Muscle-Bone Interaction
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Table 5
Correlation Between the 6-Month Changes in Measured Parameters and Changes in Calf Muscle CSA in the Active Group Using the Post Hoc Analysis
Change (%) vs Change (%) in Calf Muscle CSA R_P_ Tibia stiffness 0.85 .033 \* Tibia trabecular BV/TV 0.91 .011 \* Tibia trabecular thickness 0.38 .46 Tibia trabecular number 0.92 .0082 \* Tibia trabecular separation −0.94 .0057 \* Tibia trabecular plate-to-rod ratio 0.70 .12 Tibia trabecular BMD 0.44 .38 Tibia cortical porosity −0.44 .38 Tibia cortical density 0.29 .57 Hip BMD 0.26 .62 Lumbar spine BMD 0.19 .72 PTH 0.31 .55
BMD, bone mineral density; BV/TV, bone volume/total volume; CSA, cross-sectional area; PTH, parathyroid hormone.
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Effect of PTH on Cortical Bone
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Location Dependence of Mechanical Stimulation Effect
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Discussion
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Acknowledgments
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