Abstract: TH-PO616
Impaired Leg Muscle Mitochondrial Oxidative Capacity by Phosphorus-31 Magnetic Resonance Spectroscopy (31P MRS) Is Associated with Lower Physical Functioning in CKD
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
- Vargas, Chenoa R., UC Davis Internal Medicine, Davis, California, United States
- Howard, John, University of California Davis Medical Center, Sacramento, California, United States
- Roshanravan, Baback, University of California Davis, Davis, California, United States
- Gamboa, Jorge, Vanderbilt University, Nashville, Tennessee, United States
- Patel, Kushang V., 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, University of Washington, Seattle, Washington, United States
- Kestenbaum, Bryan R., University of Washington, Seattle, Washington, United States
Background
Maintaining functional independence is the top health priority reported by patients living with CKD. Impaired mitochondrial function is hypothesized to be a key mechanism underlying mobility limitation in 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 measured mitochondrial oxidative capacity of the tibialis anterior leg muscle (ATPmax) during exercise recovery using 31P MRS in 57 participants (38 CKD and 19 controls). We evaluated physical function by self-reported physical functioning-10 (PF-10 of the KDQOL) and performance on the Timed Up and Go (TUG) test. Statistical models adjusted for age, sex, waist/hip ratio, and maximal leg strength.
Results
Participants were 62 ±14years old and 32% had diabetes. GFRcrcysc in the CKD group was 38 ±19ml/min compared to 98 ±15 in controls. Among participants with CKD, lower muscle ATPmax correlated with slower TUG performance (r=-0.42; p=0.009) and lower PF-10 score (Figure). Results did not change after adjustment. Addition of ATPmax to the adjusted model weakened the association of CKD with physical functioning (PF-10) score by 50% (Figure) and TUG performance by 46% compared to controls.
Conclusion
Direct measurements of leg skeletal muscle mitochondrial capacity are associated with objective and subjective measures of physical functioning in patients with CKD. Mitochondrial impairment may contribute to mobility limitation in CKD.
Funding
- NIDDK Support