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Lower limb hemodynamics in hemodialysis patients with sarcopenia: A clinical and computational biomechanics study
Yuyun Wu1, Chong Chen2, Huaihong Yuan3
1Department of Nephrology, Institute of Kidney Diseases, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Background And Objectives:
Sarcopenia has a high incidence in hemodialysis patients and is closely associated with abnormal lower limb hemodynamics. This study aimed to identify the differences in lower limb arterial hemodynamics between hemodialysis patients with and without sarcopenia using a combined clinical and computational approach.
Methods:
Thirty-eight maintenance hemodialysis patients were divided into sarcopenia and control groups according to the AWGS 2019 criteria. Their ultrasound data were collected for the construction of lumped parameter models to analyze hemodynamic parameters that are difficult to measure clinically.
Results:
Patients in the sarcopenia group had significantly lower body weight and BMI than the controls (p = 0.008, p < 0.001). The mean blood flow in the femoral artery was also significantly reduced in the sarcopenia group (5.7 ± 1.6 mL/s vs. 4.5 ± 1.6 mL/s, p = 0.043), whereas no significant difference was found in the blood flow of the distal calf arteries. Simulation results indicated that the reduction in femoral inflow stems from a widespread increase in vascular resistance across the lower limb musculature rather than distal remodeling alone. By incorporating parameters associated with weight, the sarcopenia CVH-adjusted model showed reasonable agreement with group-averaged clinical hemodynamics and revealed that hypovolemia effectively counteracts the hypertensive effects of vascular stiffening. Furthermore, hydraulic power analysis showed a reduction in energy transmission efficiency, linking macrovascular changes to microcirculatory risks.
Conclusion:
These findings suggest that sarcopenic vasculopathy acts as a widespread hemodynamic disorder, in which proximal energy attenuation may further promote muscle wasting.
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