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The patient was discharged after 16 days with full recovery of renal function and stable hemoglobin

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Mechanistically, SLC25A39 deficiency induced mitochondrial dysfunction, characterized by excessive mitochondrial reactive oxygen species (ROS), reduced membrane potential, diminished adenosine triphosphate (ATP) synthesis, aberrant mitochondrial permeability transition pore (mPTP) opening, and cytochrome c release