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Urinary N-acetyl-beta-D-glucosaminidase in epileptic children treated with antiepileptic drugs
L Csáthy1, A V Oláh, B Clemens
1Department of Paediatrics, County Teaching Hospital, H-4043 Debrecen, Bartók B 2-26, Hungary. lcsathy@mail.datanet.hu
Insights
Prolonged use of antiepileptic drugs may harm kidney function in children, even at normal doses. Combined therapies and longer treatment durations increase the risk of tubular damage, necessitating regular kidney function screening.
Area of Science:
- Pediatric Nephrology
- Clinical Pharmacology
- Epileptology
Background:
- Epilepsy affects millions of children worldwide.
- Antiepileptic drugs (AEDs) are crucial for seizure control.
- Long-term effects of AEDs on pediatric renal health require investigation.
Purpose of the Study:
- To assess the impact of extended AED use on renal function in pediatric patients.
- To identify potential risk factors associated with AED-induced nephrotoxicity.
Main Methods:
- Prospective study involving 72 children (3-18 years) with epilepsy.
- Analysis of monotherapy vs. combined AED therapy over 1-13 years.
- Measurement of urinary N-acetyl-beta-D-glucosaminidase (NAG) activity as a marker of tubular damage.
Main Results:
- Elevated urinary NAG activity observed in 33 patients, indicating tubular dysfunction.
- Higher incidence of abnormal NAG indices in children on combined AED therapy compared to monotherapy.
- Significant correlation between duration of AED therapy and NAG indices.
Conclusions:
- Chronic AED use can impair pediatric tubular function, even with therapeutic plasma concentrations.
- Combined AED therapy and prolonged treatment duration are associated with increased renal risk.
- Routine screening of renal tubular function is recommended for children on long-term AEDs.
Aim:
To investigate the effect of prolonged use of antiepileptic drugs on renal function in children.
Methods:
Prospective study of 72 children (aged 3-18 years) with epilepsy, on either monotherapy (n = 44) or combined therapy (n = 28). The length of treatment varied from 1 to 13 years. Drugs used were valproic acid, carbamazepine, ethosuximide, clonazepam, clobazepam, and vigabatrin.
Results:
In 65 patients plasma concentrations of the drugs were in the therapeutic range. In the remaining seven, plasma concentrations were slightly high. In 33 patients urinary N-acetyl-beta-D-glucosaminidase (NAG) activity was raised. The incidence of pathological NAG indices was significantly higher in the combined therapy group than in the monotherapy group. There were also significant differences in the NAG indices of patients depending on the duration of therapy.
Conclusions:
Results suggest that chronic use of some antiepileptic drugs-in spite of normal blood concentrations-may alter tubular function, and the dysfunction may result in clinical symptoms. Therefore, we recommend screening of tubular function in these patients.
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