“…Orellanine causes severe non-glomerular renal injury by unknown mechanisms (11,21). Renal biopsy in affected patients reveals interstitial fibrosis and acute tubular necrosis without glomerular injury (11,17,19).…”
Section: Orellaninementioning
confidence: 98%
“…Amanita smithiana, common in the Pacific Northwest of the United States and British Columbia, causes a similar syndrome (14,15). The responsible toxin is a heat-stable bipyridyl orellanine, 2,2= bipyridine-3, 3=, 4, 4=-tetrol-1,1=-dioxide or 3,3=,4,4=-tetrahydroxy-2,2=-bipyridine-N,N=-dioxide (16,17). Although the polypeptides cortinarin A and B also have been considered toxic components, Prast et al concluded that peptides are most likely secondary metabolites of orellanine and play no role in mushroom toxicity (16,18).…”
Mushrooms are ubiquitous in nature. They are an important source of nutrition, however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, whereas foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I reviewed the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and presented an overview of the cyclopeptide-containing mushroom class. Part II is focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.
“…Orellanine causes severe non-glomerular renal injury by unknown mechanisms (11,21). Renal biopsy in affected patients reveals interstitial fibrosis and acute tubular necrosis without glomerular injury (11,17,19).…”
Section: Orellaninementioning
confidence: 98%
“…Amanita smithiana, common in the Pacific Northwest of the United States and British Columbia, causes a similar syndrome (14,15). The responsible toxin is a heat-stable bipyridyl orellanine, 2,2= bipyridine-3, 3=, 4, 4=-tetrol-1,1=-dioxide or 3,3=,4,4=-tetrahydroxy-2,2=-bipyridine-N,N=-dioxide (16,17). Although the polypeptides cortinarin A and B also have been considered toxic components, Prast et al concluded that peptides are most likely secondary metabolites of orellanine and play no role in mushroom toxicity (16,18).…”
Mushrooms are ubiquitous in nature. They are an important source of nutrition, however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, whereas foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I reviewed the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and presented an overview of the cyclopeptide-containing mushroom class. Part II is focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.
“…Antkowiak et al described the chemical structure of orellanine as 3,3,4,4-tetrahydroxy-2,2-bipyridine-N,N-dioxide [11]; later, Holmdahl et al supported the authenticity of this chemical structure by 1 H-NMR and 13 C-NMR spectra analyses [12].…”
Cortinarius orellanus (Fries) and C. rubellus (Cooke), which were formerly also known as C. speciosissimus, are poisonous mushrooms containing the toxin orellanine and several degradation products of orellanine, including orelline and orellinine. Mass intoxication by poisonous mushrooms was observed in Poland in 1952Poland in -1957. In 1957, the cause of these outbreaks was described by Grzymala as poisoning by a member of the Cortinarius family. The toxin orellanine was first isolated from C. orellanus by Grzymala in 1962; the chemical structure of orellanine was later determined to be 3,3,4,4-tetrahydroxy-2,2-bipyridine-N,N-dioxide. Poisoning with C. orellanus and C. rubellus has a very specific character. The first symptoms of intoxication usually do not appear until 2 -3 days after ingestion, but in some cases intoxication appears after three weeks. The target organ for the toxin is the kidney. Histologically, it is easy to record the specific damage. The presence of degradation products of orellanine in kidney can be confirmed chromatographically, suggesting that the cause of poisoning is orellanine. However, the presence of orellanine in the blood of intoxicated persons has not been directly detected. A specific model was developed by Brondz et al. for the detection of orellanine, orelline, and orellinine in animal stomach fluids [2][3][4]. The hypothesis that the fungal toxin orellanine as a diglucoside can be transported from the digestive system by the blood to the kidney could not be supported. The toxin orellanine as a diglucoside is very unstable in an aqueous acidic environment. However, in the present study, it was possible to record an additional substance in animal stomach fluids using GC-MS after ingestion of C. rubellus. This substance, which has been named rubelline, is part of a toxic mixture in C. orellanus and C. rubellus and is closely related to orellanine. The structure of rubelline is more suitable than orellanine for absorption from the digestive tract and for transport in the blood. The presented hypothesis is that rubelline is absorbed in the digestive tract and transported in the blood to the kidney, where it is biotransformed to orellanine and accumulated to toxic levels. The process of biotransformation is in itself also damaging for the kidney and liver. GC-MS instrumentation enables the separation of substances in biological samples and in the extract from C. rubellus. The GC-MS with SMB technique was used to record the mass ion and to record a detailed fragmentation picture.
“…This is in turn due to the tubulo-interstitial nephritis caused by damage to the tubular cells. In case of more severe poisoning, the patient becomes anuric after around 1 week [4]. Fig.…”
Section: Introductionmentioning
confidence: 99%
“…Due to the lag-phase between intake and symptoms, there are no signs of toxins in blood [19]. Suggested therapies during the years have been hemodialysis, hemoperfusion, corticosteroids and anti-oxidant therapies with highly varying and inconclusive results [4, 20, 21]. Regarding long-term effects of the intoxication, there are only a few reports following transplantation [17, 22].…”
BackgroundAccidental intake of mushrooms of the Cortinarius species (deadly webcap) may cause irreversible renal damage and the need for dialysis or transplantation. The species is found in forests of Northern Europe, Scandinavia and North America and may be mistaken for other edible mushrooms. The highly selective nephrotoxic compound of the mushroom is called orellanine. Very little is known about the long-term effects of the nephrotoxin.MethodsWe identified patients who ingested deadly webcap in the period of 1979 to 2012. Informed consent and medical records were obtained for 28 of the 39 cases that occurred during the 34-year period. A case control group was also studied based on sex, age and initiation of dialysis or transplantation.ResultsThe average age at time of the accidental intake was 40 ± 3 (n = 28) years. 64% of patients were male, and 22 of 28 patients developed acute kidney injury requiring dialysis. Serum creatinine peaked at 1 329 ± 133 μmol/l, and serum urea was 31 ± 3.5 mmol/l. No signs of acute damage were present in any other organ. The average time of follow-up was 16.9 ± 2.1 years (1.24–34.3 years, n = 28). 15 patients were transplanted and 3 also had a second graft. At follow-up, 23 patients were alive, and five had died at ages of 67 ± 5 (range 54–84). The outcome was similar in the case control group with 6 deaths in 20 patients.ConclusionWe conclude that the long-term prognosis for patients poisoned by deadly webcap who lost their renal function is not different compared to other patients in active uremic care.
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