Abstract: TH-PO615
Lower Kidney Function Is Associated with Impaired Leg Skeletal Muscle Mitochondrial Oxidative Capacity
Session Information
- Health Maintenance, Nutrition, Metabolism - I
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Health Maintenance, Nutrition, and Metabolism
- 1300 Health Maintenance, Nutrition, and Metabolism
Authors
- Howard, John, University of California Davis Medical Center, Sacramento, California, United States
- Vargas, Chenoa R., University of California Davis Medical Center, Sacramento, California, United States
- Roshanravan, Baback, University of California Davis Medical Center, Sacramento, California, United States
- Gamboa, Jorge, Vanderbilt University, Nashville, Tennessee, United States
- Himmelfarb, Jonathan, Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
- de Boer, Ian H., Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
- Conley, Kevin, Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
- Kestenbaum, Bryan R., Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
Background
Evidence suggests abnormal uremic environment may contribute to mobility limitation by impairing muscle mitochondrial function. We tested the association of kidney function with in vivo muscle mitochondrial oxidative capacity among patients with CKD.
Methods
The Muscle Mitochondrial ENergetics and Dysfunction (MEND) study was designed to evaluate determinants and consequences of skeletal muscle mitochondrial functioning in CKD. We recruited 57 participants (38 CKD and 19 controls) from a clinic-based population. We measured mitochondrial oxidative capacity of the tibialis anterior leg muscle (ATPmax) during exercise recovery using 31Phosphorus magnetic resonance spectroscopy. We determined associations of GFRcrcysc with ATPmax by using multivariable linear regression adjusting for age, sex, waist/hip ratio, and diabetes.
Results
Participants were 62 ±14years old with 32% female and 32% prevalence of diabetes (33% in controls). GFRcrcysc in the CKD group was 38 +19ml/min compared to 98 ±15 in controls. Mean ATPmax was 0.6 ±0.16mM/sec in CKD group and 0.8 ±0.18 in controls. After adjustment, CKD was associated with 0.18mM/sec lower (95% CI 0.27, 0.09; P<0.001) ATPmax. Diabetes was associated with 0.12mM/sec lower (95%CI 0.23, 0.02; P=0.02) ATPmax compared non-diabetes after adjustment. In continuous analysis, each 10ml/min/1.73m2 lower eGFRcrcysc was associated with a 0.03mM/sec lower ATPmax (95% CI 0.04, 0.01; P<0.001) (Figure). Among those with GFRcrcysc<60, correlates with ATPmax included bicarbonate level (r=0.39, p=0.02), C-reactive protein (r=-0.31, P=0.07), albuminuria (r=-0.33, P=0.05), and phosphorus (r=-0.21, p=0.2).
Conclusion
Lower kidney function and diabetes are associated with direct in vivo measurements of leg muscle mitochondrial oxidative capacity.
Funding
- NIDDK Support