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Amanita Phalloides Nephrotoxicity — ESENeph MCQ

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HardAcute Kidney InjuryAmanita Phalloides NephrotoxicityESENeph

A 30-year-old woman develops AKI with anuric renal failure after ingesting Amanita phalloides (death cap mushroom). Liver failure is also present. What is the mechanism of renal injury?

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Correct answer: C — Direct mushroom toxin nephrotoxicity to proximal tubules (amatoxin causes RNA polymerase II inhibition and cell death) plus hepatorenal syndrome component

Amanita phalloides contains amatoxins (alpha-amanitin) which are concentrated in the kidney (renal excretion) and directly toxic to proximal tubular cells through RNA polymerase II inhibition, blocking mRNA synthesis and causing cell death. The renal injury is compounded by concurrent hepatorenal syndrome from fulminant liver failure. Management is supportive: aggressive IV fluids, N-acetylcysteine (hepatoprotective), Silibinin (may block hepatocyte amatoxin uptake), RRT for AKI, and liver transplant assessment for hepatic failure.

Reference: NPIS – Amanita Poisoning; Enjalbert et al 2002 – Amatoxin Toxicity