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1/5. Acute tubular necrosis induced by high level of cyclosporine A in a lung transplant.

    We report a case of acute accidental cyclosporine A intoxication in a lung transplant patient. The intoxication led to renal failure due to acute tubular necrosis, which was partially reversible. A review of the literature on the renal consequences of cyclosporine A intoxication is given.
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2/5. paraquat-induced fanconi syndrome.

    The ingestion of paraquat, a non-selective herbicide, can be fatal in humans. paraquat is toxic to multiple organs, including the kidney, heart, gastrointestinal tract and central nervous system. Although paraquat has been established as one cause of acute tubular necrosis, fanconi syndrome presenting as severe hypophosphataemia after paraquat intoxication has not been reported. Here, we report the case of a 44-year-old Korean woman who presented with generalized proximal tubular dysfunction including aminoaciduria, phosphaturia and glycosuria after paraquat intoxication. We found that severe hypophosphataemia induces deep drowsiness. Renal biopsy findings indicated the presence of acute tubular necrosis that may be reversible.
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3/5. Impairment of organ function after oral ingestion of refined petrol.

    After oral ingestion of 600 ml of refined petrol a 23-year-old male developed multiple organ failure. Acute renal insufficiency due to nephrotoxic tubular necrosis requiring hemodialysis was a major manifestation. Moreover, respiratory failure, seizures, hemolysis, disseminated intravascular coagulation, liver damage and erosions of mucous membranes occurred. The patient subsequently recovered completely. In spite of the poor absorption from the gastrointestinal tract and the high first-pass effect in the liver, massive petrol intoxication may lead to reversible multisystemic lesions.
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keywords = intoxication
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4/5. Prenatal and early postnatal intoxication by inorganic mercury resulting from the maternal use of mercury containing soap.

    A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3-month-old black boy in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal, ocular and haematological defects may have resulted from exposure to mercury during foetal life and the 1-month lactation period due to the extensive use of inorganic mercury containing cosmetics by the mother.
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5/5. Acute nephropathy of organotin compounds.

    Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.
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