# Is Amanita phalloides Nephrotoxicity due to Mitochondrial Toxicity?

## TL;DR

A 43-year-old patient developed kidney damage after eating Amanita phalloides, with evidence of mitochondrial changes but preserved COX function.

## Contribution

The study provides the first evidence of mitochondrial toxicity in Amanita phalloides-induced kidney injury.

## Key findings

- Kidney injury showed mitochondrial swelling and reduced cristae under electron microscopy.
- TOM20 expression was significantly decreased compared to ischemic acute tubular injury.
- COX function was preserved despite mitochondrial damage.

## Abstract

Amanita phalloides-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 Amanita phalloides. 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 Amanita phalloides elicits acute tubular injury via mitochondrial damage, possibly through a pathway that spares COX function.