To the editor:
Harvesting and intake of wild mushrooms causes a significant number of poisonings, particularly in autumn. A patient with a mixed syndrome of hepatic and renal failure following intake of mushrooms from the species Amanita phalloides and Cortinarius orellanus is reported. No description of any poisoning showing such an association has been found in the literature. A 74-year old male patients with an unremarkable history attended the emergency room for intractable vomiting and diarrhoea. The patient reported to have taken mushrooms 12-15 hours before. Physical examination showed an acceptable general condition and haemodynamic stability. Laboratory test results included: urea 89 mg/dL, creatinine 3.4 mg/dL, Na 137 mmol/L, K 4 mmol/L, GOT 1406 IU/L, GPT 1170 IU/L, LDH 1319 IU/L. Coagulation: PAI 71%, APTT 43.4 sec, INR 1.24. Complete blood count: Hb 18 mg/dL, haematocrit 53.3%, WBCs 11,200/mm3 (N 78%). Urine: Na 30 mmol/L, K 66 mmol/L, urea 16.3 g/L, creatinine 155.4 mg/dL. Acute renal failure due to volume depletion and hepatic failure secondary to mushroom intake were diagnosed, and the patients was admitted to the intensive care unit. Treatment was started with penicillin G sodium, activated charcoal, water and electrolyte replacement, pyridoxine, vitamin K, traxenamic acid, and fresh plasma. The reference liver transplant unit was contact because of suspected poisoning by Amanita phalloides. The cytolysis pattern and coagulation changes started to improve on the third day of stay at the ICU, and the patient was discharged to the gastroenterology ward. On the fourth day of stay at the ward (7 days since mushroom intake), creatinine levels of 4.2 mg/dL (as compared to a previous value of 1.5 mg/dL) were reported to the nephrology department. Urine: Na 95 mmol/L, K 49.08 mmol/L, urea 14.94 g/L, creatinine 100 mg/dL, protein 0.5 g/L, no RBCs. Normal complete blood count without eosinophilia, and normal C3 and C4. A further evaluation ruled out a prerenal cause, nephrotoxic agents, and an obstructive cause (by ultrasonography). Since a relationship with mushroom intake was suspected, mushrooms were analysed by an expert mycologist, who identified several species, including Amanita phalloides and Cortinarius orellanus. Support measures were started and an adequate water balance was ensured. Patient remained asymptomatic with a preserved urine output and maximum creatinine levels of 7.1 mg/dL with metabolic acidosis. Liver enzymes and coagulation were normal. Renal replacement therapy was not required at any time, and kidney function gradually improved until basal creatinine levels of 2 mg/dL were achieved. These levels have been maintained to date.
Mushroom poisoning is classified into two large groups based on whether the time elapsed from intake to symptom occurrence is shorter or longer than 6 hours. Poisonings caused by the Amanita and Cortinarius genera belong to the latter group (2-21 days). The potential occurrence of mixed syndromes due to the concomitant intake of several species, as occurred in our case, should also be taken into account.
Species from the genus Cortinarius have two types of toxins, cortinarins and orellanines. Orellanines show a high renal tropism, inhibiting protein synthesis in tubular cells. Orellanine degradation produces oxygen free radicals and glutathione depletion. Orellanines remain in renal tissue for up to 6 months after intake.
Renal failure occurs in 30%-75% of all poisonings depending on individual sensitivity and the amount ingested. End-stage chronic renal failure occurs in approximately one third, temporal haemodialysis is required in another third in which total or partial recovery of kidney function is subsequently achieved, and the remaining third experience no renal damage.
Non-specific gastrointestinal symptoms initially occur. These are associated to urinary frequency, that is occasionally followed by an oliguric phase with onset of uremic symptoms. Hepatic damage is rare, and some cases of transient cytolysis have only been reported.
Renal biopsy mainly shows interstitial nephritis with tubular necrosis and infiltration by lymphocytes, plasma cells, and PMNs with no glomerular involvement.
There is no specific antidote. Treatment should be supportive and symptomatic. Haemodialysis and plasmapheresis are not effective for toxin removal because of the long symptom-free period involved in late diagnosis. However, good results have been reported in some cases when performed within 5 days of poisoning. Use of corticoids and N-acetylcysteine for its antioxidant and glutathione-donating effect has been reported, but their efficacy is controversial.
