Abstract: SA-PO049

Not Such a Fun-gi

Session Information

Category: Acute Kidney Injury

  • 003 AKI: Clinical and Translational


  • Blonsky, Rebecca, Cleveland Clinic, Cleveland, Ohio, United States
  • Herlitz, Leal C., Cleveland Clinic, Cleveland, Ohio, United States
  • Anvari, Evamaria, Cleveland Clinic, Cleveland, Ohio, United States

Amanita Phalloides is a poisonous mushroom known as death cap, found in central Europe and the northeastern United States. Its toxicity arises from amatoxins, which when ingested can lead to severe gastrointestinal (GI) malady, renal and liver failure and in some cases, death.


A 55-year-old Nepali male presented with nausea and vomiting for four days. He and his family were in a park and they saw mushrooms similar to those in Nepal which they collected and consumed. They then developed abdominal pain, nausea, vomiting and diarrhea. As their symptoms persisted, they sought care and it was found they had ingested amanita phalloides.
Initial labs showed a creatinine (Cr) of 4.67 mg/dL, AST 1551 U/L, ALT 1103 U/L and total bilirubin 1.8 mg/dL. The patient was admitted to intensive care and nephrology was called for acute kidney injury (AKI). Urinalysis and renal ultrasound were normal but urine microscopy showed many unusual crystals, but no signs of acute tubular necrosis (ATN).
The patient was treated with intravenous fluids, N-acetyl cysteine, octreotide and was enrolled in a trial using silibinin derived from Silybum marianum (milk thistle) being studied in amatoxin ingestion. With treatment, liver function improved and renal function normalized and was discharged after three days with a Cr of 0.8 mg/dL.
Ten days later he returned complaining of edema, shortness of breath, anorexia and bitter taste. Labs showed BUN of 45 mg/dL and Cr of 8.69 mg/dL. Renal biopsy was done and showed ATN. After a total of two sessions of intermittent hemodialysis, he regained renal function and was discharged with a Cr of 3.95 mg/dL. On three month follow up, he achieved partial renal recovery to a stable Cr of 1.7 mg/dL.


AKI frequently occurs in amatoxin ingestion. It causes pre-renal azotemia as well as direct tubular toxicity through the amatoxins’ inhibition of RNA polyermase II causing ATN. Though not well described, renal injury could be as a result of crystal deposition. Renal failure has also been reported following normalization of liver function. This pathophysiology is not well defined and has been hypothesized to be a result of the formation of free radicals causing ATN as the toxin is cleared after treatment. Patients who have ingested amanita phalloides require close follow up even with normalization of hepatic and renal function.