Breslau N A, McGuire J L, Zerwekh J E, Pak C Y
J Clin Endocrinol Metab. 1982 Aug;55(2):369-73. doi: 10.1210/jcem-55-2-369.
Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 +/- 2 to 226 +/- 8 meq/day (mean +/- SEM), urinary Ca rose from 110 +/- 14 to 167 +/- 16 mg/day, serum parathyroid hormone (PTH) increased from 20 +/- 1 to 22 +/- 1 muleq/ml, serum 1,25-(OH)2D rose from 38 +/- 4 to 51 +/- 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 +/- 0.03 to 0.49 +/- 0.03 (P less than 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 +/- 0.1 to 9.8 +/- 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 +/- 12 to 245 +/- 11 meq/day) and urinary Ca (271 +/- 48 to 305 +/- 43; P less than 0.05). However, there were no increases in serum PTH (13 +/- 1 to 11 +/- 1 muleq/ml), serum 1,25-(OH)2D (44 +/- 1 to 40 +/- 6 pg/ml), or intestinal Ca absorption (0.41 +/- 0.03 to 0.42 +/- 0.05). Corrected serum Ca decreased from 9.4 +/- 0.2 to 8.6 +/- 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.
早期研究表明,口服钠(Na)负荷可使既往正常钙尿症患者出现高钙尿症,还可能增加肠道钙(Ca)吸收。为探究肠道钙吸收增加的原因,我们在盐负荷前后同时测量了甲状旁腺功能、血清1,25 - 二羟维生素D [1,25 - (OH)₂D]以及肠道47Ca的吸收分数。11名正常受试者和2名甲状旁腺功能减退症术后患者接受了为期10天的每日10毫当量钠、400毫克钙的饮食,随后是另一个10天的阶段,在此期间每日相同饮食补充240毫当量钠。在每个阶段的最后3天进行测量。正常受试者中,尿钠排泄量从7±2增加至226±8毫当量/天(均值±标准误),尿钙从110±14增加至167±16毫克/天,血清甲状旁腺激素(PTH)从20±1增加至22±1微当量/毫升,血清1,25 - (OH)₂D从38±4增加至51±7皮克/毫升,肠道47Ca吸收分数从0.39±0.03增加至0.49±0.03(所有变化P均小于0.05)。校正总蛋白后的血清钙未改变(9.9±0.1至9.8±0.1毫克/分升)。接受维生素D治疗的甲状旁腺功能减退症患者尿钠(20±12至245±11毫当量/天)和尿钙(271±48至305±43;P小于0.05)也有增加。然而,血清PTH(13±1至11±1微当量/毫升)、血清1,25 - (OH)₂D(44±1至40±6皮克/毫升)或肠道钙吸收(0.41±0.03至0.42±0.05)均未增加。校正后的血清钙从9.4±0.2降至8.6±0.2毫克/分升。我们得出结论,在正常受试者中,钠诱导的肾性高钙尿症伴有1,25 - (OH)₂D合成增加和肠道钙吸收增强。由于这种适应性机制在两名甲状旁腺功能减退症患者中未出现,提示由PTH介导。