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[Threshold for bicarbonate in epileptic children in treatment with anticonvulsant drugs (author's transl)]
Insights
Anticonvulsant drugs in epileptic children can lower the renal bicarbonate threshold, leading to biochemical rickets. This suggests a non-parathyroid hormone-mediated mechanism affecting kidney function in these patients.
Area of Science:
- Pediatric Nephrology
- Clinical Biochemistry
- Pharmacology
Context:
- Epileptic children on anticonvulsant drugs exhibit unique metabolic profiles.
- Anticonvulsant therapy is associated with potential renal and bone metabolism disturbances.
- Understanding these disturbances is crucial for managing long-term health in pediatric epilepsy.
Purpose:
- To investigate the renal handling of bicarbonate and mineral metabolism in ambulatory epileptic children treated with anticonvulsant drugs.
- To compare biochemical parameters between epileptic children and a control group.
- To explore potential mechanisms underlying observed metabolic alterations.
Summary:
- Epileptic children on anticonvulsants showed a significantly lower renal threshold for bicarbonate, low calcemia, and elevated alkaline phosphatase compared to controls.
- No differences were found in urinary cyclic AMP, phosphate, or calcium excretion.
- A negative correlation existed between renal bicarbonate threshold and serum phosphate, and between urinary cyclic AMP and treatment duration.
Impact:
- The findings suggest that the reduced renal bicarbonate threshold in these patients is a non-parathyroid hormone-mediated phenomenon.
- This research highlights potential renal tubular dysfunction associated with anticonvulsant therapy in children.
- It provides insights into the biochemical characteristics of rickets in this specific pediatric population, distinct from deficiency rickets.
Abstract:
The study comprised 31 ambulatory epileptic children aged 1,5-14 years (mean: 7.37), receiving treatment with anticonvulsant drugs. Authors found that renal threshold for bicarbonate was inferior when compared to control group (mean = 21.3 mEq/l., SD = 1.75; mean = 25.34 mEq/l., SD = 1.29; p less than 0.0001), low calcemia (mean = 9.12 mg./dl., SD = 0.51; mean = 9.43, SD = 0.45; p less than 0.01) and elevated alkaline phosphatase (mean = 212.6 mU/ml., SD = 75.9; mean = 127.4, SD = 50.2; p less than 0.01). No significant difference in urinary excretion of cyclic AMP, phosphate or calcium was observed. Nineteen patients who had subnormal threshold (inferior to -2 SD in the control group) when compared with control group, had: low calcemia (p less than 0.01), high alkaline phosphatase (p less than 0.0001) and a similar urinary cyclic AMP, calciuria and phosphaturia. A negative correlation between renal threshold to bicarbonate and serum phosphate (r = -0.49, p less than 0.01) and a negative correlation between the urinary cyclic AMP and the duration of treatment (r = -0.42, p less than 0.05) was found. It is commented that although in deficiency rickets, proximal tubular acidosis is due to secondary hyperparathyroidism, in their patients despite they had biochemical characteristics of rickets, low calcemia and elevated alkaline phosphatase, the descent of renal threshold to bicarbonate is a nonparathoromone mediated phenomenon.