JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
post-ingestion, and all received temporary hemodialysis for several weeks before regaining normal renal function. 6 The laboratory ranges of the presenting serum biomarkers of acute renal failure included a blood urea nitrogen (BUN) of 72-91 mg/ dL and a creatinine level of 12-13.9 mg/dL. 6 In addition to A. proxima in Europe and A. smithiana in North America, a delayed onset of acute renal failure was reported from Asia following the consumption of other species of Amanita mushrooms, specifically A. pseudoporphyria in Japan (2003) and A. punctata in Korea (2015). 7, 8 Recently, Kirchmair and coinvestigators in Lisbon, Portugal, used thin layer chromatography and Amanita smithiana toxin to test several other Amanita species for the suspected nephrotoxin. 26 The Amanita smithiana nephrotoxin, now known as allenic norleucine, was detected in samples of A. boudieri, A. gracilor, and A. echinocephala collected by Portuguese mushroom hunters. 27 The authors concluded that the intoxications produced by these Amanita mushrooms would resemble the same toxidromes that followed the consumption
of A. smithiana with a delayed onset of acute, reversible renal failure and mild hepatitis with transaminitis. 27 The mechanisms of allenic norleucine’s toxicity are unknown, but it is a suspected direct nephrotoxin. 27 It causes renal epithelial cell necrosis when cultured with renal tubular epithelium in vitro and does not deplete glutathione like orellanine. 27 Lastly, there are two species of myotoxic mushrooms, (1) Tricholomaequestre, first reported as poisonous in France in 2001, and (2) Russula subnigricans, first reported as poisonous in China in 2015, that can cause potentially fatal rhabdomyolysis resulting in acute renal failure following consumption. 4,28 Tricholoma equestre , the yellow knight mushroom, was formerly considered edible and its toxicity was dose-related and associated with an increasing number of mushroom meals. 4 Russula subnigricans was commonlymistaken for a less poisonous species that shared the same coniferous forest habitat in China, Russula nigricans; but its myotoxicity was not dose-related. 4, 28 In 2001, Bedry and coinvestigators reported 12 cases of delayed rhabdomyolysis with three fatalities in patients who had consumed consecutive meals of the edible wild mushroom, Tricholomaequestre (synonym T. flavovirens ), harvested frompine forests in coastal southwestern France. 4 Following a prodrome of afebrile fatigue andmyalgia 24-72 hours after the last mushroom meal, most (n = 8) patients described a worsening weakness and stiffness of their legs accompanied by facial erythema, mild nausea without vomiting, profuse sweating, and darkening urine color over three to four days. 4 Rhabdomyolysis was later confirmed by significantly elevated creatine kinase (CK) levels without any laboratory evidence of cardiac or hepatic injury. 4 Muscle biopsies in six patients demonstrated histopathological evidence of acute myopathy. 4 In all but three of the patients, the serum CK levels normalized and most symptoms resolved, but muscular weakness persisted for weeks. 4 In the three fatal cases, the serum CK levels continued to rise and all patients developed hyperthermia up to 42° C, cardiac arrhythmias, renal dysfunction (elevated serum creatinine, BUN, and potassium), and cardiovascular collapse. 4 Autopsies demonstrated myocardial lesions identical to the muscle biopsy lesions in one patient, renal lesions in one patient, and no histopathological evidence of hepatic damage in all cases. 4 The investigators later administered boiled extracts of T. equestre to mice who developed significant increases in CK levels and postmortem histopathological evidence of muscle damage compared to control mice who received boiled extracts from another species of mushroom and maintained normal CK levels and muscle biopsies. 4 The investigators concluded that since most patients with toxic rhabdomyolysis survived, a genetic muscular susceptibility may have triggered the fatal dose-related myotoxic effects after an ingestion threshold of mushrooms was exceeded. 4 The authors cautioned physicians of the possibility of rhabdomyolysis after the repeated consumptions of T. equestre mushrooms. 4 The treatment for T. equestre -induced rhabdomyolysis is supportive. The mushroom myotoxin remains unidentified.
Figure 3: Amanita smithiana, or Smith’s Amanita, is native to the Pacific Northwest of the United States and Canada where it has been mistaken for the edible pine or matsutake mushroom, Tricholoma magnivalere . It has a large white plano-convex cap with unattached free gills and a thick, shaggy white stem with a torn or absent ring or annulus. Although gas- trointestinal toxicity occurs 5-8 hours after ingestion, delayed acute renal failure typically requiring hemodialysis will occur 5-6 days after ingestion. Source: Wikimedia commons (public domain). Photographer: Sava Krstic.
166 J La State Med Soc VOL 169 NOVEMBER/DECEMBER 2017
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