amanitins and Kidney-Diseases

Among fungal toxins causing organ damage in the human body, amatoxins and orellanine remain exceptional. Amatoxins, a group of bicyclic octapeptides occurring in some Amanita, Galerina and Lepiota species, induce deficient protein synthesis resulting in cell death, but might also exert toxicity through inducing apoptosis. Target organs are intestinal mucosa, liver and kidneys. Poisoning will result in dehydration and electrolyte derangement, liver necrosis and possibly kidney damage. In established poisoning the mainstay of treatment is optimum symptomatic and supportive care. No specific treatment is available, but some pharmaceuticals, like silibinin, benzylpenicillin and acetylcysteine, might have a role in limiting the extent of hepatic damage. Orellanine is a nephrotoxic bipyridine N-oxide found in some Cortinarius species. Its mechanism of action is not fully understood, but it has been shown to inhibit protein synthesis and to generate free oxygen radicals. As early symptoms often are lacking or vague, poisoning may initially be overlooked or misinterpreted and the patients usually present with established renal damage. Supportive care is the only therapeutic option. Tricholoma equestre might contain a myotoxin and repeated ingestion may cause significant rhabdomyolysis. Ingestion of Amanita smithiana and A. proxima has been reported to result in kidney damage. Gyromitrin, a toxic compound that is converted to hydrazines in the stomach, occurs in some Gyromitra species. It is mainly neurotoxic, but may also induce moderate hepatic damage and haemolysis.

Topics: 2,2'-Dipyridyl; Acetaldehyde; Amanitins; Basidiomycota; Humans; Kidney Diseases; Mushroom Poisoning; Mycotoxins; Rhabdomyolysis

Topics: Amanita; Amanitins; Chemical and Drug Induced Liver Injury; Female; Humans; Kidney Diseases; Middle Aged; Mushroom Poisoning

In human beings, poisoning by the deathcup mushroom causes renal lesions in addition to extremely severe liver damage. It is known from animal experiments that silymarin, a polyhydroxyphenylchromanone, is capable of counteracting this alpha-amanitin-induced liver damage. The purpose of the present work was to ascertain whether renal damage could be induced in rats by giving alpha-amanitin, and whether silymarin would have any effect on such renal damage. The fact that alpha-amanitin produces pathological changes in the kidneys and that these lesions can be almost completely prevented by pretreating rats with silymarin has now been amply demonstrated by biochemical and histological techniques alike.

Topics: Amanitins; Animals; Flavonoids; Hematocrit; Kidney Diseases; Male; Rats; Silymarin; Time Factors