Renal Tubular Function in Patients Receiving Anticonvulsant Therapy: A Long‐Term Study

Verrotti, Alberto; Greco, Rita; Pascarella, Raffaella; Matera, Vincenzo; Morgese, G; Chiarelli, Francesco

doi:10.1111/j.1528-1157.2000.tb00118.x

Cited by 27 publications

(21 citation statements)

References 13 publications

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“…It is known that NAG is an early marker in several renal diseases, such as hypertension, diabetic nephropathy, toxicity, nephritic syndrome, and chronic renal failure; [6][7][8][9] this, there is no correlation between SV and time-related tubular dysfunctions, according to the present findings.…”

Section: Discussioncontrasting

confidence: 76%

“…According to the results of several clinical trials, it has been accepted that a raised amount of the enzyme in urine is an early marker of tubular injury. [6][7][8][9] Malondialdehyde (MDA) is a highly reactive aldehyde that is formed from the peroxidation of fatty acids. An increase in the urinary MDA excretion was reported as an indicator of hepatic and renal cell damage.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Sodium Valproate on Renal Functions in Rats

et al. 2006

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In recent years, it has been reported that sodium valproate occasionally can cause renal tubular impairment. This study was designed to demonstrate the renal tubular and glomerular functions in rats given sodium valproate as monotherapy, as well as to determine any reversibility of dysfunctions. Female rats were randomly allocated to three groups: group 1 received sodium valproate 500 mg/kg/d intraperitoneal for six weeks; after the same injection period, group 2 was housed for another six weeks, after which laboratory investigations were completed; and group 3 served as a control group made up of 20 healthy rats living in same condition without any treatment. Serum ALT, total protein, uric acid, ALP, phosphorus, sodium levels, and urine Ca/cr ratio were significantly different between groups 1 and 3 (p < 0.025), but this difference was not seen between groups 2 and 3. On the other hand, other parameters such as TRP, Ccr, NAG, and MDA were not significantly different among the three groups ( p > 0.025) These results suggest that SV does not have a significant dose- or time-related side effect on renal functions. Minor biochemical dysfunctions related to long-term sodium valproate therapy is reversible, and the minimal renal fibrosis that showed histopathologically is not clinically important. The renal tissues of rats are known to show similar metabolic and histological patterns with human renal tissues. No renal dysfunction was expected in humans because there were no clinically statistically significant renal side effects in this study.

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Section: Discussioncontrasting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Effects of Sodium Valproate on Renal Functions in Rats

et al. 2006

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“…Verrotti et al 17) reported significantly higher α1-microglobulin levels in patients treated with CBZ compared to controls. This confirms that the evaluation of α1-microglobulin excretion can help detect impaired proximal tubular function in patients receiving CBZ for antiepileptic therapy.…”

Section: Discussionmentioning

confidence: 99%

Side Effects of Antiepileptic Drugs on Renal Tubular Function in Childhood-onset Epilepsy

Endo

Fujita

Fuchigami

et al. 2012

Nichidai Igaku Zasshi

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Valproic acid-induced Fanconi syndrome in severely disabled, developmentally retarded, and non-ambulatory epileptic children has gradually become more widespread. Although the mechanism is unclear, renal involvement has been suspected. We investigated the effect of antiepileptic drugs and ambulatory state on renal tubular function in epileptic patients. We studied 77 patients who were treated at the Department of Pediatrics and Child Health, Nihon University Itabashi Hospital. The patients were divided into three groups according to antiepileptic drug administration and ambulatory state: severely disabled patients taking mainly valproic acid (9 cases), ambulatory patients taking valproic acid monotherapy (34 patients), and ambulatory patients taking carbamazepine monotherapy (34 patients). Laboratory analysis of renal tubular function showed that β 2-microglobulin levels were increased significantly in severely disabled patients. In addition, α 1-microgulobulin levels were increased significantly in ambulatory patients receiving carbamazepine monotherapy but not valproic acid. These results suggest that carbamazepine affects renal tubular function to a greater extent than valproic acid in ambulatory non-handicapped patients with epilepsy. We propose the importance of monitoring urinary α 1-microgulobulin and β 2-microglobulin levels in epileptic children for the early detection of subclinical renal tubular dysfunction.

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“…In epileptic patients, significant increases of urinary α1-microglobulin and Hex activity have been described, suggesting a proximal tubular dysfunction produced by the administered anticonvulsant drugs (39,40). It is interesting that in our patients in which the determination of the urinary excretion of total Hex activity and porphyrins was performed, a significant correlation between them was found (r = 0.790, P = 0.006).…”

Section: Discussionmentioning

confidence: 67%

Effect of Antiepileptic Drugs on the Urinary Excretion of Porphyrins in Non-porphyric Subjects

Tutor-Crespo¹,

Hermida²,

Tutor³

2005

J Pharmacol Sci

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Abstract. The action of some anticonvulsant drugs as the causal agents of attacks of acute porphyria has been widely documented in the literature. However, little attention has been paid to the effect of these drugs on the urinary excretion of porphyrins in non-porphyric subjects. In a sample of 82 epileptic patients treated with phenobarbital (n = 54), phenytoin (n = 64), carbamazepine (n = 33), and valproate (n = 8), the daily doses were expressed according to a drug score that would reflect the capacity of these drugs as enzymatic inducers when administered in polytherapy. A significantly increased urinary excretion of D-glucaric acid (DGA) and porphyrins was found in this group of patients (P<0.001), with coproporphyrin being the major fraction in all cases (>60%). Urinary DGA had a highly significant correlation with the drug score (r = 0.783, P<0.001); however, no significant correlations were found between the urinary porphyrins and DGA (r = 0.005) or the drug score (r = 0.053). Neither was any significant relationship found between the urinary porphyrins and the serum activity of 5'-nucleotidase (r = 0.066) or the presence of a cholestasis objectivized through the presence of the isoform of γ-glutamyltransferase with β-globulins electrophoretic mobility. However, in a group of 10 patients a significant correlation was found between the urinary excretion of porphyrins and β-N-acetylhexosaminidase (r = 0.790, P<0.01). Therefore, it does not appear that the liver enzyme induction, or even a subclinical cholestasis, produced by the antiepileptic drugs administered to these patients may serve to explain the increase in the urinary excretion of porphyrins. A possible renal origin is proposed for the increase of urinary porphyrins in these cases.

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Renal Tubular Function in Patients Receiving Anticonvulsant Therapy: A Long‐Term Study

Cited by 27 publications

References 13 publications

Effects of Sodium Valproate on Renal Functions in Rats

Effects of Sodium Valproate on Renal Functions in Rats

Side Effects of Antiepileptic Drugs on Renal Tubular Function in Childhood-onset Epilepsy

Effect of Antiepileptic Drugs on the Urinary Excretion of Porphyrins in Non-porphyric Subjects

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