Early detection of renal impairment among epileptic children on anti-epileptic medication

ABSTRACT

Epilepsy is defined as a paroxysmal electrical discharge affecting a group of neurons, starting in one part of the brain but often spreading to become a generalized abnormality. Despite the recent advances in surgery, the management of epilepsy depends mainly on medication. Treatment with anti-epileptic drugs [AED] was reported to cause changes in hepatic and renal functions. Nephrotoxicity is suggested by evidence of glomerular and/or tubular dysfunction. Glomeruiar damage may present as hematuria, increased 24 hour urinary protein excretion, elevated blood urea nitrogen [BUN] and serum creatinine and lowered creatinine clearance. Tubular dysfunction is reflected by low urine specific gravity and increased levels of urinary enzymes. The present study was conducted at Damanhour Medical National Institute [DMNI] at Beheira Governorate. It aims at the early detection of renal impairment among epileptic children on AED therapy. It comprises sixty epileptic newly diagnosed patients aged 5 -16 years suffering from different types of epilepsy. They were divided into three groups according to the type of medication. Patients in-group 1 were treated with Carbamazine [CBZ], group 2 was treated with Valproate [VPA], and group 3 was treated with Phenantoin [PHE]. Patients were compared to thirty healthy children [group 4] not suffering from any disease. All groups were compared as regards age, nutritional status and renal function to provide a baseline before the start of the study. The same procedures were repeated six months later to evaluate the renal function after the treatment with AED. At the end of the study, no clinical manifestation of renal dysfunction was observed following AED therapy. Furthermore, our results revealed no significant difference between blood urea [P=0.91], blood urea nitrogen [P=0.91], serum creatinine [P=0.66], creatinine clearance [P=0.72], routine urine analysis, and 24 hour urinary albumin in all patients before and after AED therapy. On the other hand, there was a significant increase in urinary NAG in the three groups of patients after AED therapy. This increase was highest in patients receiving VPA monotherapy [2.34 +/- 2.00 U/g versus 1.68 +/- 1.76U/g and 1.9121. +/- 0U/g creatinine for the patients treated with CBZ and with PHE respectively]. The three groups did not differ as regards NAG level after AED therapy, but there was a significant difference in dMG/24h between the three groups at P=0.01