SUMMARY:
Aim: To assess the effects of anti‐epileptic drugs on renal tubular function.
Methods: Urinary N‐acetyl‐β‐D‐glucosaminidase activity was measured in 114 epileptic children (mean age 5.6 ± 1.1 years) who were undergoing monotherapy with valproate (n = 46), carbamazepine (n = 34), lamotrigine (n = 13) and combined therapy with valproate+carbamazepine (n = 21).
Results: The urinary N‐acetyl‐β‐D‐glucosaminidase index of valproate (P< 0.01), carbamazepine (P< 0.05) and polytherapy group (P< 0.01) were significantly elevated when compared with that of the control group. No significant difference in N‐acetyl‐β‐D‐glucosaminidase levels was found between the lamotrigine group and the control subjects. We found that the distribution of the N‐acetyl‐β‐D‐glucosaminidase values of patients depended significantly on the length of therapy (P< 0.01). The level of urinary excretion of N‐acetyl‐β‐D‐glucosaminidase was significantly higher in the patients who were taking long‐term treatment (>10 years) with valproate, carbamazepine and combined therapy than those taking therapy shorter than 10 years (P< 0.01). The mean serum concentrations of valproate and carbamazepine were 68.7 ± 17.44 µg/mL and 5.41 ± 1.23 µg/mL, respectively. There was a significant correlation between the serum concentration of valproate and urinary N‐acetyl‐β‐D‐glucosaminidase levels (r= 0.44, P < 0.01). There was also a significant correlation between the serum concentration of carbamazepine and N‐acetyl‐β‐D‐glucosaminidase excretion (r= 0.52, P < 0.01).
Conclusion: The present study demonstrated that in patients treated with valproate and carbamazepine, an impairment of tubular function can be present, whereas lamotrigine does not cause any significant change.