Is Nephrotoxicity due to Mitochondrial Toxicity?

-related kidney toxicity is poorly documented and remains to be elucidated. Herein, we describe the case of a 43-year old patient who presented with severe liver failure following the ingestion of . Although liver injury subsided following the administration of N-acetyl cystein and silibinin, the patient subsequently developed KDIGO stage 3 acute kidney injury. Histopathological examination of the kidney displayed moderate tubular injury characterized by dilated tubular lumens and flattening of the tubular epithelium on optic microscopy. Electron microscopy showed mitochondrial changes including swelling and decreased number of cristae. Immunofluorescence for the key mitochondrial protein TOM20 found significantly decreased expression compared with ischemic acute tubular injury. Despite these changes, histoenzymology showed preserved succinate cytochrome c oxidase (COX) expression, suggesting that mitochondrial complex IV function was maintained. Our findings suggest that elicits acute tubular injury via mitochondrial damage, possibly through a pathway that spares COX function.