Stoller Marshall L, Chi Thomas, Eisner Brian H, Shami Gina, Gentle Donald L
Department of Urology, School of Medicine, University of California-San Francisco, San Francisco, California, USA.
J Urol. 2009 Mar;181(3):1140-4. doi: 10.1016/j.juro.2008.11.020. Epub 2009 Jan 18.
We investigated the effects of supplemental dietary sodium on risk factors for urinary stone disease in stone forming patients with hypocitraturia.
Ten patients diagnosed with recurrent isolated hypocitraturic calcium urolithiasis were identified. Baseline 24-hour urinalysis was performed with patients on their regular diet, including citrate replacement with 20 mEq potassium citrate 3 times per day. Strict daily dietary logs were kept for a 7-day period, during which patients had normal oral intake and potassium citrate replacement. Patients then received supplemental sodium chloride for 1 week (1 gm orally 3 times per day), in addition to their regular diets and potassium citrate supplementation. Dietary logs were continued and 24-hour urinalysis was performed at the end of 1 week of supplemental sodium. Risk factors for urinary stone disease were compared using the Student t test and ANOVA.
Two patients were unable to comply with sodium supplementation based on 24-hour urinalysis and, therefore, they were excluded from study. The remaining 8 patients were analyzed. Patients on supplemental dietary sodium demonstrated significantly increased mean urinary voided volume (933 ml per day above baseline, p <0.05) and mean urinary sodium excretion (66 mEq per day above baseline, p <0.05). There was no statistically significant change in urinary calcium, oxalate or uric acid. The urinary supersaturation relative risk ratio decreased for calcium oxalate stones (0.93 vs 0.63, p <0.05), while those of brushite, struvite and uric acid were not different before vs after supplemental sodium.
Dietary sodium supplementation resulted in an increased voided urine volume and decreased the relative risk supersaturation ratio for calcium oxalate stones in patients with a history of hypocitraturic calcium oxalate nephrolithiasis. Urinary calcium excretion as well as other urine parameters that are risk factors for nephrolithiasis was not changed. Sodium restriction may be inappropriate in patients with hypocitraturia and recurrent urinary stones. Sodium supplementation may be beneficial in these patients because it results in voluntary increased fluid intake.
我们研究了补充膳食钠对枸橼酸盐尿减少的结石形成患者尿路结石病危险因素的影响。
确定了10例诊断为复发性孤立性低枸橼酸钙性尿路结石的患者。对患者进行常规饮食下的基线24小时尿液分析,包括每天3次用20毫当量柠檬酸钾替代枸橼酸盐。严格记录7天的每日饮食日志,在此期间患者口服摄入正常且补充柠檬酸钾。然后,患者在常规饮食和补充柠檬酸钾的基础上,接受1周的氯化钠补充(每天口服1克,分3次)。继续记录饮食日志,并在补充钠1周结束时进行24小时尿液分析。使用学生t检验和方差分析比较尿路结石病的危险因素。
根据24小时尿液分析,2例患者无法遵守钠补充方案,因此被排除在研究之外。对其余8例患者进行了分析。补充膳食钠的患者平均排尿量显著增加(比基线水平每天多933毫升,p<0.05),平均尿钠排泄量增加(比基线水平每天多66毫当量,p<0.05)。尿钙、草酸盐或尿酸没有统计学上的显著变化。草酸钙结石的尿过饱和相对风险比降低(0.93对0.63,p<0.05),而补充钠前后透钙磷石、鸟粪石和尿酸的尿过饱和相对风险比没有差异。
补充膳食钠可使枸橼酸盐尿减少的草酸钙肾结石病史患者的排尿量增加,并降低草酸钙结石的相对风险过饱和比。尿钙排泄以及其他作为肾结石病危险因素的尿液参数没有改变。对于枸橼酸盐尿减少和复发性尿路结石患者,限制钠摄入可能不合适。补充钠可能对这些患者有益,因为它会导致自愿增加液体摄入量。