HHS Public Access Author manuscript Author Manuscript
Am J Kidney Dis. Author manuscript; available in PMC 2016 October 14. Published in final edited form as: Am J Kidney Dis. 2016 October ; 68(4): 658–659. doi:10.1053/j.ajkd.2016.05.011.
CKD and Muscle Mitochondrial Energetics Baback Roshanravan, MD MSPH MS1, Bryan Kestenbaum, MD MS1, Jorge Gamboa, MD PhD3, Sharon A. Jubrias, PhD2, Ernest Ayers, MSPH1, Laura Curtin, BA1, Jonathan Himmelfarb, MD1, Ian. H. de Boer, MD MS1, and Kevin E. Conley, PhD2
of Washington Kidney Research Institute, Seattle, WA
of Washington, Seattle, WA
University Medical Center, Nashville, TN Chronic kidney disease (CKD) leads to the retention of uremic solutes that disrupt skeletal muscle function1 leading to reduced physical performance and mobility limitation2. Disruption of muscle mitochondrial energetics in CKD may precede the onset of detectable functional limitations. In particular, reduced coupling of ATP production to oxygen consumption (P/O ratio) within mitochondria of skeletal muscle indicates oxidative stress, impaired metabolism, and reduced exercise efficiency3–6. Comprehensive analysis of skeletal muscle mitochondrial energetics in CKD patients has been limited by lack of precise, real-time, non-invasive techniques.
We used in vivo magnetic resonance spectroscopy and optical spectroscopy (31P MRS/OS) procedures to measure resting mitochondrial energetics for the first time among non-diabetic CKD patients (GFR