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Delayed Onset Acute Renal Failure Associated with Amanita Pseudoporphyria Hongoingestion

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Delayed Onset Acute Renal Failure Associated with Amanita Pseudoporphyria Hongoingestion å¡ CASE REPORT å¡ Delayed Onset Acute Renal Failure Associated with Amanita pseudoporphyria HongoIngestion Yoichi IWAFUCHI, Takashi MORITA*, Hideyuki KOBAYASHI, Kensaku KASUGA, Kazuhisa ITO, Osamu NAKAGAWA,Kaoru KUNISADA, Shigeru MlYAZAKI** and Akira KAMIMURA Abstract smithiana. A 66-year-old manwith diabetes developed acute renal Case History failure after ingestion of Amanita pseudoporphyria Hon- go. Laboratory data showed acute nonoliguric renal fail- In October 2000, a 66-year-old man was admitted; he had ure. A renal biopsy showed acute tubular necrosis with been well until several days before admission when he no- glomerular minor abnormalities. He received hemodialy- ticed general fatigue, facial edema and appetite loss. Six sis treatment for 3 weeks and his renal function normal- months before admission his renal function was normal and ized 2 months after admission. Wediscuss the differences urinary protein was negative. Twoweeks before admission in acute renal failure caused by possible toxins of he picked two mushroomsof Amanita pseudoporphyria Amanita pseudoporphyria Hongo from that caused by Hongo (Fig. 1) with other absolutely edible mushrooms and other poisonous mushrooms. ate them. Nobody else ate the mushroom except for him. He (Internal Medicine 42: 78-81, 2003) was aware of severe fatigue from the following day, but there were no severe gastointestinal symptoms.Onthe day Key words: acute renal failure, Amanita pseudoporphyria of admission, he was seen by a physician and pretibial edema Hongo, mushroompoisoning, nephrotoxin, alle- and renal failure (creatinine 18.0 mg/dl) were pointed out. nic norleucine (2-amino-4, 5-hexadienoic acid) He had a ten-year history of diabetes, and he had taken glibenclamide for five years, but recently he had not taken any other drugs before the occurrence of the abnormal find- ings. Introduction On examination his blood pressure was 186/80 mmHg, pulse 82/min, temperature was 37.4°C. He had gained 5 kg Severe acute renal failure caused by mushroompoisoning in weight in the previous four weeks. Hewas not anemic nor is rare in Japan. Nephrotoxicity is most commonlyreported icteric. His heart and lungs were normal, and lymph nodes due to amatoxin poisoning in Japan as well as in Europe and were not palpable. Noexanthema was observed but moderate North America. In Europe delayed onset renal failure caused peripheral edema was present. No neurological abnormalities by orellanine poisoning has also been reported. Recently in werenoted. the Pacific Northwest, Amanitasmithiana has been reported Urinalysis showed a 1+ test for protein, a 1+ test for glu- to contain other nephrotoxinsand several cases of acute renal cose and a 1+ test for occult blood; sediment showed 3-5 failure have been reported following ingestion of the mush- erythrocytes, 3-5 leukocytes, and 5-10 hyaline casts per room. Amanita smithiana is possibly being mistaken for the high-power field. Urinary protein was 0.2 g/24 hour and glu- popular matsutake, or "pine mushroom"Tricholoma magni- cose was 1.5 g/24 hour. The urine p2 microglobulin level velare, to which it bears a superficial resemblance. was 20,640 mg/dl. Stool and urine cultures were negative. Wedescribe the first case report with delayed onset acute Hematocrit was 36.2%, the hemoglobin concentration was renal failure after ingestion of Amanita pseudoporphyria 13.5 g/dl; the platelet count was 157,000/mm3, and the leuko- Hongo that contains the same nephrotoxin as Amanita cyte count was 9,200/mm3.The serum urea nitrogen level From the Department of Internal Medicine, Koseiren Sanjo General Hospital, Sanjo, *the Department of Pathology, Shinrakuen Hospital, Niigata and **the Department of Internal Medicine, Kidney Center, Shinrakuen Hospital, Niigata Received for publication June 17, 2002; Accepted for publication December 2, 2002 Reprint requests should be addressed to Dr. Yoichi Iwafuchi, the Department of Internal Medicine, Koseiren Sanjo General Hospital, 5-1-62 Tsukanome, Sanjo 955-0055 78 Internal Medicine Vol. 42, No. 1 (January 2003) ARFDue to MushroomPoisoning % .Xt \1 <y'. *mv: Figure 2. Renal biopsy reveals prominent tubulointestial le- sions as shown at higher magnification in Fig. 3. A glomeruli appears normal (Periodic acid-silver methenamine stain, x60). Figure 1. Amanita pseudoporphyria Hongo: the mushroomsthat the patient ingested. hospital day, a renal biopsy was performed to elucidate the cause of acute renal failure. Renal histology revealed was 148.7 mg/dl, creatinine, 16.48 mg/dl; uric acid, 8.0 tubulointerstitial lesions and glomerular minor abnormalities. mg/dl; total protein, 6.9 g/dl; and albumin, 4.0 g/dl. The Someproximal tubular cells were vacuolated and the nuclei serumaspartate aminotransferase level was17 IU/Z; alanine were pycnotic. A mitotic figure was also found. In some di- aminotransferase, 37 IU/Z; lactate dehydrogenase, 1,123 IU/Z; lated tubules epithelial cells were stripped off, and the alkaline phosphatase, 166 IU/Z; P-glutamyltranspeptidase, 1 8 lumina were filled with cellular debris. Patchy interstitial cel- IU/Z; and creatine phosphokinase, 459 IU/Z. The serum lular infiltrates, either polynuclear or mononuclear cells were myoglobin level was 496 ng/ml and the urinary myoglobin observed (Figs. 2, 3). level was 980 ng/ml. The serum sodium level was 124 At that time a diagnosis of acute renal failure due to acute mmol/Z, potassium, 6.8 mmol/Z; and chloride, 81 mmol/Z. The tubular necrosis was made. Although rhabdomyolysis ex- glycosylated hemoglobin Ale level was 7.8%. The C reac- isted, it was mild, and not considered as the main cause of tive protein level was 1.87 mg/dl; immunogloblin (Ig) G, renal failure. From the findings of the renal biopsy he had 1,308 mg/dl; IgA, 219 mg/dl; IgM, 84 mg/dl and ferritin, 131 not undertaken steroid therapy. He received homodialysis ng/ml. The total complement level was 74.9 IU/Z; C3, 123 treatment three times a week during the following three mg/dl; and C4, 36 mg/dl. Rheumatoid factor, antistreptolysin weeks. Urine output was over 1,000 ml/24 hour during his O, hepatitis B virus surface antigen, hepatitis C virus anti- admission and the creatinine level improved rapidly. Onthe body, human immunodeficiency virus antibody, antinuclear antibody and antineutrophil cytoplasmic antibody were all negative. Anarterial blood sample in room air disclosed that the partial oxygen pressure level was 101.9 mmHg;partial dioxide carbon pressure, 19.3 mmHg; HCO3, 9.3 mmol/Z and pH 7.293. There were no cryoglobulin in the serum. The / prothrombin time and activated thromboplastin time were both normal. There were no abnormal findings in ECG. His chest X-ray showed mild cardiomegaly. On computed tomography, slight swelling of the kidneys was observed (longitudinal axis: 12.5 cm). Simple type of diabetic retino- pathy was present. Hemodialysis was started on the day of admission. He is 'V** à"å ."- passably conversant with mushrooms. Whenshown a picture of the type of mushroom he ate (Fig. 1) he told us ingestion of Amanita pseudoporphyria Hongo would be poisonous. Other causes, such as dehydration and drug use, could not be Figure 3. Interstitial cell infiltration is observed near a dilated found, so wesuspected that acute renal failure was caused by stripped tubule filled with cellular debris (D). Some tubular ingestion of Amanita pseudoporphyria Hongo. As his clini- cells are vacuolated (one of them is indicated by an arrow) (HE cal course was atypical for mushroompoisoning, on the 6th stain, x260). Internal Medicine Vol. 42, No. 1 (January 2003) 79 Iwafuchi et al 23rd hospital day the patient was discharged without any Table 1. Selected Poisonous Mushrooms and Their Toxins subjective symptoms.Weobserved himat the out-patient de- (1-6) partment; his creatinine level normalized 2 months after ad- Genus and species Toxins mission (creatinine 0.9 mg/dl). I. Cyclopeptide-containing mushrooms Discussion Amanita virosa Amatoxins* Amanita verna Phallotoxins* The clinical course, laboratory findings and renal histo- Amanita phalloides Virotoxins * logical findings of this patient led to a diagnosis of acute Galerina species renal failure due to acute tubular necrosis associated with Lepiota species II. Monomethylhydrazine-containing mushrooms Amanita pseudoporphyria Hongo ingestion. Gyromitra species Monomethlhydrazine Mushroomcollecting is popular in Japan and sometimes III. Muscarine-containing mushrooms mild mushroompoisoning is reported. Severe acute renal Amanitamuscaria Muscarine failure associated with mushroomingestion is very rare, but Amanita pantherina some kinds of nephrotoxins have been reported (Table 1). Clitocybe dealbata Somecases of acute renal failure associated with amatoxin- Cliocybe dilatata producing mushrooms, such as Amanita virosa, Amanita Cliocybe illudens verna, Amanita phalloides, Galerina species and Lepiota Most Inocybe species species, have been reported in Japan, Europe and North IV. Coprine-containing mushrooms America (1, 2). Especially Amanita phalloides is known as Coprinus atramentarius Coprine "the death cap", which causes severe illness of the liver and V. Ibotenic acid- and muscimol-containing mushrooms renal failure. This type of organ failure is very severe, with Amanita gemmata Ibotenic acid a mortality rate of more than 50% (1, 2). In addition Amanita muscaria Muscimol Amanita pantherina orellanine intoxication has also been reported associated with VI. Psilocybin-containing mushrooms acute renal failure in Europe and Japan (1, 2). Orellanine is Psilocybe
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