• Patrick L West, Janet Lindgren, and B Zane Horowitz.
• Oregon Health and Science University, Oregon Poison Center, USA. westp@ohsu.edu
• J Med Toxicol. 2009 Mar 1; 5 (1): 32-8.

IntroductionIn the Pacific Northwest a new pattern of mushroom ingestion has emerged, attributed to Amanita smithiana, in which renal failure has been the predominant manifestation.Case ReportA 55-year-old male ate 3 raw wild mushrooms in a salad and had onset of severe nausea and vomiting within 6 hours. His vital signs were unremarkable. His labs were significant for a BUN of 14 mg/dL (5.0 mmol/L), and a creatinine of 1.0 mg/dL (88 umol/L), transaminases were elevated with an AST of 56 U/L (nl 9-40) and an ALT of 131 U/L (nl 14-72). Treatment was initiated with N-acetyl cysteine, penicillin, and milk thistle extract on the presumption that this was an amanitin-toxin containing mushroom. He developed acute renal failure that was not responsive to our treatment. Dialysis started on day 4 with a creatinine of 6.5 mg/dL, which peaked on day 7 at 10.2 mg/dL. We were able to obtain a positive mushroom identification by a mycologist as Amanita smithiana. The patient was discharged from the hospital for outpatient dialysis on day 10 and dialysis catheter was removed 39 days after ingestion with a creatinine of 1.4 mg/dL (123.8 umol/L).DiscussionAmanita smithiana mushroom poisoning presents within 6 hours of ingestion with GI toxicity, and develops delayed onset of renal insufficiency over the first 1 to 4 days. The early hospitalization of this case allowed a profile of the onset of liver and renal injury. Mild elevation of hepatic transaminases occurred on presentation and peaked 24 hours after the ingestion. Renal injury was detected 1 day after presentation, and progressed to require hemodialysis by 4 days postingestion. This pattern of delayed-onset renal toxic mushroom ingestion is emerging among mushroom ingestions in Western North America.

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