Abstract: FR-PO162

Muscle Mitochondrial Energetics, Objective Muscle Fatigability, and Symptoms of Fatigue in CKD

Session Information

  • Mitochondriacs and More
    November 03, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Nutrition, Inflammation, and Metabolism

  • 1401 Nutrition, Inflammation, Metabolism

Authors

  • Roshanravan, Baback, Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
  • Liu, Sophia, University of Washington, Seattle, Washington, United States
  • Ali, Amir Safi, University of Washington, Seattle, Washington, United States
  • Gamboa, Jorge, Vanderbilt University, Nashville, Tennessee, United States
  • de Boer, Ian H., Division of Nephrology and Kidney Research Institute, University of Washington, Seattle, Washington, United States
  • Himmelfarb, Jonathan, 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
  • Conley, Kevin, University of Washington, Seattle, Washington, United States
Background

People with chronic kidney disease (CKD) often report symptoms of fatigue. Impaired skeletal muscle mitochondrial function due to the abnormal uremic milieu of CKD may contribute to muscle fatigability and symptoms of fatigue.

Methods

We performed a cross-sectional analysis of 30 participants from the Muscle Mitochondrial ENergetics and Dysfunction (MEND) study. Persons were excluded from MEND if they used medications effecting mitochondrial metabolism, had mobility disability, or weighed >300 pounds. We measured mitochondrial capacity of the tibialis anterior muscle as ATPmax using 31P magnetic resonance spectroscopy. We determined the force time integral (an objective measure of muscle fatigability) and assessed fatigue symptoms using the FACIT-F questionnaire.

Results

Mean GFR was 35 ±15 ml/min; mean age was 61 ±14yr; 53% were female, and 23% had diabetes. Lower muscle ATPmax was associated with lower force time integral (indicating greater fatigability) (figure 1; P=0.007) and greater symptoms of fatigue after adjustment (figure 2; P=0.013).

Conclusion

Muscle mitochondrial capacity measured by ATPmax is associated with objective fatigability and subjective symptoms of fatigue in CKD patients. These findings are the first connecting impaired human skeletal muscle mitochondrial energetics in CKD with functional and clinical measures.

Figure 1. Association of ATPmax with muscle fatigability.

Figure 2. Association of ATPmax with self-reported fatigue.

Funding

  • NIDDK Support