Valproic acid (VPA) is a potent antiepileptic drug (AED) for generalized and partial epilepsy in adults and children ( 3, 4). Drugs are the most common cause of acquired FS, including aminoglycosides, various chemotherapeutics, antiepileptic drugs, and iron chelators ( 2). Fanconi syndrome can be triggered by different causes, including hereditary, idiopathic, and acquired. The median time to resolution of FS after discontinuation of drug therapy was 3 months (range 0.25–18).įanconi syndrome (FS) is a systemic proximal tubular dysfunction characterized by proteinuria, glycosuria, phosphateuria, generalized hyperaminoaciduria, hypokalemia, hypophosphatemia, and type II renal tubular acidosis ( 1). Decreased percent total reabsorption of phosphate (%TRP) found in 94.1% of patients, and increased fractional excretion of uric acid (FEUA) were found in 100% of patients. Urinalysis revealed glucosuria (96.1%), proteinuria (100.0%), generalized hyperaminoaciduria (100.0 %), β2 macroglobulin (100.0%).

Blood tests revealed hypokalemia (69.2%), hypophosphatemia (98.0%), and hypouricemia (93.3%).

Pathological fractures (25.9%), unexplained fever (11.1%), muscle weakness (9.3%), and edema (9.3%) were the most common symptoms, while 18 patients were diagnosed in incidental laboratory tests. The median duration of VPA treatment was 4 years (range 0.7–15.5).

The patients had a median age of 7 years (range 2–34 years), had severely disabled (87.0%), tube feeding (64.8%), and received an average of 1.8 medications other than VPA. A total of 29 articles including 54 patients (28 males and 24 females) were included.

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