de Manueles J, Macías Núñez J F, Rodríguez Commes J L, Blázquez J, Santos Borbujo J, Salazar V
An Esp Pediatr. 1981 Mar;14(3):175-82.
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.
该研究纳入了31名年龄在1.5至14岁（平均7.37岁）的门诊癫痫儿童，他们正在接受抗惊厥药物治疗。作者发现，与对照组相比，这些儿童的碳酸氢盐肾阈值较低（平均值分别为：对照组21.3 mEq/l，标准差1.75；研究组25.34 mEq/l，标准差1.29；p<0.0001），血钙水平较低（平均值分别为：对照组9.43mg/dl，标准差0.45；研究组9.12mg/dl，标准差0.51；p<0.01），碱性磷酸酶升高（平均值分别为：对照组127.4 mU/ml，标准差50.2；研究组212.6 mU/ml，标准差75.9；p<0.01）。未观察到环磷酸腺苷、磷酸盐或钙的尿排泄有显著差异。与对照组相比，19名阈值低于正常水平（低于对照组-2个标准差）的患者有：低血钙（p<0.01）、高碱性磷酸酶（p<0.0001）以及相似的尿环磷酸腺苷、尿钙和尿磷。发现碳酸氢盐肾阈值与血清磷酸盐之间呈负相关（r=-0.49，p<0.01），尿环磷酸腺苷与治疗持续时间之间呈负相关（r=-0.42，p<0.05）。评论指出，虽然在营养性佝偻病中，近端肾小管酸中毒是由继发性甲状旁腺功能亢进引起的，但在他们的患者中，尽管有佝偻病的生化特征、低血钙和碱性磷酸酶升高，但碳酸氢盐肾阈值的下降是一种非甲状旁腺激素介导的现象。
