Otsuka T, Sunaga Y, Hikima A
Department of Pediatrics, Gunma University School of Medicine, Maebashi, Japan.
Brain Dev. 1994 Nov-Dec;16(6):437-40. doi: 10.1016/0387-7604(94)90003-5.
We investigated potential renal functional impairment induced by chronic use of anti-epileptic drugs (AEDs) in 79 epileptic children. They were divided into five groups: valproic acid (VPA) monotherapy where the serum concentration (SC) of VPA was no less than 60 micrograms/ml (VPA [SC > or = 60]) (15 cases), VPA monotherapy where the SC VPA was less than 60 micrograms/ml (VPA [SC < 60]) (29 cases), phenobarbital monotherapy (PB) (7 cases), carbamazepine monotherapy (CBZ) (16 cases), and polytherapy containing VPA (12 cases). Urinalysis (proteinuria and hematuria) and serum creatinine were normal except for two cases of proteinuria and two cases of hematuria. The level of urinary excretion of N-acetyl-beta-glucosaminidase (u-NAG) was high in 29% of all patients, and 47% of VPA (SC > or = 60), 38% of CBZ, 25% of polytherapy, and 24% of VPA (SC < 60) groups. There was a significant positive correlation between serum concentration of VPA and u-NAG/urinary creatinine (u-Cr). The level of guanidinoacetic acid (u-GAA) excreted in the urine was normal except in one patient. U-NAG/u-Cr may be a more sensitive marker than u-GAA/u-Cr for renal functional impairment in AED therapy.
