CKD leads to retention of uremic solutes that disrupt skeletal muscle function,1 reducing physical performance and limiting mobility.2 Disruption of muscle mitochondrial energetics in CKD may precede detectable functional limitations. In particular, reduced coupling of ATP production to O2 consumption within mitochondria of skeletal muscle indicates oxidative stress, impaired metabolism, and reduced exercise efficiency.3-6 Comprehensive analysis of skeletal muscle mitochondrial energetics in patients with CKD has been limited by the lack of precise real-time noninvasive techniques.