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Paraquat‐induced Fanconi syndrome
Author(s) -
GIL HYO W,
YANG JONG O,
LEE EUN Y,
HONG SAE Y
Publication year - 2005
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2005.00437.x
Subject(s) - paraquat , medicine , ingestion , glycosuria , tubulopathy , fanconi syndrome , gastrointestinal tract , aminoaciduria , kidney , urinary system , hypophosphatemia , pathology , necrosis , acute tubular necrosis , endocrinology , diabetes mellitus , urine , biology , biochemistry
SUMMARY: 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.