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With one of the highest mitochondrial densities in the body, the kidneys consume approximately 10% of total oxygen while constituting 0.5% of body mass. Renal respiration is linear to solute extraction, linking oxidative metabolism directly to tubular function. This fundamental role of mitochondria in renal health may become an “Achilles heel” under duress. Acute kidney injury (AKI) related to each major class of stressor - inflammation, ischemia, and toxins - exhibits early and prominent mitochondrial injury. The mitochondrial biogenesis regulator, PPARγ-coactivator-1α (PGC1α), may confer tubular protection against these stressors. Recent work proposes that renal PGC1α directly increases levels of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for energy metabolism that has lately been proposed as an anti-aging factor. This mini-review summarizes recent studies on AKI, PGC1α, and NAD+ that identify a direct mechanism between the regulation of metabolic health and the ability to resist renal stressors.