Sakhaee K, Ruml L, Padalino P, Haynes S, Pak C Y
University of Texas Southwestern Medical Center at Dallas 75235-8885, USA.
J Am Coll Nutr. 1996 Feb;15(1):102-6. doi: 10.1080/07315724.1996.10718572.
It has been suggested that citrate salts might enhance aluminum (Al) absorption from a normal diet, posing a threat of Al toxicity even in subjects with normal renal function. We have recently reported that in normal subjects and patients with moderate renal failure, short-term treatment with tricalcium dicitrate (Ca3Cit2) does not significantly change urinary and serum Al levels. However, we have not assessed total body Al stores in patients on long-term citrate treatment.
The objective of this study was to ascertain body content of Al non-invasively using the increment in serum and urinary Al following the intravenous administration of deferoxamine (DFO) in patients with kidney stones and osteoporotic women undergoing long-term treatment with potassium citrate (K3Cit) or Ca3Cit2, respectively.
Ten patients with calcium nephrolithiasis and five with osteoporosis who were maintained on potassium citrate (40 mEq/day or more) or calcium citrate 800 mg calcium/day (40 mEq citrate) for 2 to 8 years, respectively, and 16 normal volunteers without a history of regular aluminum-containing antacid use participated in the study. All participants completed the 8 days of study, during which they were maintained on their regular home diet. Urinary Al excretion was measured during a two-day baseline before (Days 5, 6) and for 1 day (Day 7) immediately following a single intravenous dose of DFO (40 mg/kg). Blood for Al was obtained before DFO administration, and at 2, 5 and 24 hours following the start of the infusion.
The median 24-hour urinary Al excretion (microgram/day) at baseline versus post-DFO value was 15.9 vs. 44.4 in the normal subjects and 13.3 vs. 35.7 in the patients. These values were all within normal limits and did not change significantly following DFO infusion (p = 0.003 and p = 0.0001, respectively). The median change of 17.1 micrograms/day in urinary Al in the normal subjects was not significantly different from the 18.7 micrograms/day change measured in the patient group (p = 0.30). Similarly, no change in the mean serum Al was detected at any time following the DFO infusion, either in the patient or control group (patients 4.1 to 4.3 ng/ml, controls 7.4 to 4.6 ng/ml).
The results suggest that abnormal total body retention of Al does not occur during long-term citrate treatment in patients with functioning kidneys.
有人提出柠檬酸盐可能会增加正常饮食中铝（Al）的吸收，即使在肾功能正常的受试者中也会构成铝中毒的威胁。我们最近报告，在正常受试者和中度肾衰竭患者中，用柠檬酸三钙（Ca3Cit2）进行短期治疗不会显著改变尿铝和血清铝水平。然而，我们尚未评估长期接受柠檬酸盐治疗的患者体内的铝总量。
本研究的目的是，分别对接受柠檬酸钾（K3Cit）或Ca3Cit2长期治疗的肾结石患者和骨质疏松症女性，通过静脉注射去铁胺（DFO）后血清和尿铝的增加情况，以非侵入性方式确定其体内铝含量。
10例钙肾结石患者和5例骨质疏松症患者分别参加了本研究，他们分别服用柠檬酸钾（40 mEq/天或更多）或柠檬酸钙（800 mg钙/天，40 mEq柠檬酸盐）2至8年，16名无规律使用含铝抗酸剂病史的正常志愿者也参与了研究。所有参与者均完成了为期8天的研究，在此期间他们保持日常饮食。在单次静脉注射DFO（40 mg/kg）前的两天基线期（第5、6天）及注射后1天（第7天）测量尿铝排泄量。在注射DFO前、输液开始后2、5和24小时采集血样检测铝含量。
正常受试者基线期与DFO注射后的24小时尿铝排泄中位数（微克/天）分别为15.9和44.4，患者分别为13.3和35.7。这些值均在正常范围内，DFO注射后无显著变化（分别为p = 0.003和p = 0.0001）。正常受试者尿铝中位数变化为17.1微克/天，与患者组测量的18.7微克/天变化无显著差异（p = 0.30）。同样，在DFO注射后的任何时间，患者组或对照组的血清铝均值均未检测到变化（患者组4.1至4.3 ng/ml，对照组7.4至4.6 ng/ml）。
结果表明，肾功能正常的患者在长期接受柠檬酸盐治疗期间不会出现铝在体内的异常潴留。
