Veenhuizen L, Donckerwolcke R A
Department of Pediatrics, University of Utrecht, Wilhelmina Children's Hospital, The Netherlands.
Child Nephrol Urol. 1991;11(2):69-73.
In 9 children with idiopathic hypercalciuria, an oral calcium-loading test was performed. After this calcium excretion, vitamin D levels, parathyroid hormone levels and phosphate excretion were measured during a period of calcium restriction, a period of high calcium intake and a period of low calcium intake and phosphate supplementation. In our patients, there was no correlation between calcium excretion following acute and long-term calcium loading. Phosphate excretion was normal during the periods of low and high calcium intake and there were no signs of renal phosphate leakage. Elevated levels of 1,25-dihydroxyvitamin D were found with no significant change after altering phosphate or calcium intake (95% confidence intervals for the difference in 1,25-dihydroxyvitamin D levels were -2.2-15.4 pg/ml in the period with low and high calcium intake; -19.8-28.2 pg/ml in the period with low calcium intake and extra phosphate, and -24.2-19.6 pg/ml in the period with high calcium intake and extra phosphate). These data support the hypothesis of an autonomously elevated 1,25-dihydroxyvitamin D level as pathogenetic mechanism for idiopathic hypercalciuria.
对9名特发性高钙尿症患儿进行了口服钙负荷试验。在此次钙排泄后,在钙限制期、高钙摄入期以及低钙摄入和补充磷酸盐期测量了钙排泄量、维生素D水平、甲状旁腺激素水平和磷酸盐排泄量。在我们的患者中,急性和长期钙负荷后的钙排泄之间没有相关性。在低钙摄入期和高钙摄入期磷酸盐排泄正常,且没有肾磷酸盐泄漏的迹象。发现1,25-二羟基维生素D水平升高,在改变磷酸盐或钙摄入量后无显著变化(低钙摄入期和高钙摄入期1,25-二羟基维生素D水平差异的95%置信区间为-2.2-15.4 pg/ml;低钙摄入期加额外磷酸盐时为-19.8-28.2 pg/ml,高钙摄入期加额外磷酸盐时为-24.2-19.6 pg/ml)。这些数据支持1,25-二羟基维生素D水平自主升高作为特发性高钙尿症发病机制的假说。