[Threshold for bicarbonate in epileptic children in treatment with anticonvulsant drugs (author's transl)].

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.