Department of Dermatology and Cutaneous Biology, Sidney Kimmel Medical College, Jefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA,
PXE International Center of Excellence in Research and Clinical Care, Thomas Jefferson University, Philadelphia, Pennsylvania, USA,
Nephron. 2024;148(7):480-486. doi: 10.1159/000534495. Epub 2024 Jan 23.
BACKGROUND/AIMS: Hypercalciuria is the most common identifiable risk factor predisposing to CaOx stone formation. Increased oral magnesium intake may lead to decreased CaOx stone formation by binding intestinal Ox leading to decreased absorption and/or binding urinary Ox to decrease urinary supersaturation. This study assessed the effect of oral magnesium on 24-h urine ion excretion, supersaturation, and kidney stone formation in a genetic hypercalciuric stone-forming (GHS) rat model of human idiopathic hypercalciuria.
When fed the oxalate precursor, hydroxyproline, every GHS rat develops CaOx stones. The GHS rats, fed a normal calcium and phosphorus diet supplemented with hydroxyproline to induce CaOx, were divided into three groups of ten rats per group: control diet with 4.0 g/kg MgO, low MgO diet (0.5 g/kg), and high MgO diet (8 g/kg). At 6 weeks, 24-h urines were collected, and urine chemistry and supersaturation were determined. Stone formation was quantified.
The GHS rats fed the low and high Mg diets had a significant reduction and increase, respectively, in urinary Mg compared to those fed the control diet. Dietary Mg did not alter urine Ca excretion while the low Mg diet led to a significant fall in urinary Ox. Urine supersaturation with respect to CaOx was significantly increased with low Mg, whereas urine supersaturation was significantly decreased with high Mg. There was no effect of dietary Mg on stone formation within 6 weeks of treatment.
Dietary magnesium decreases urine supersaturation but not CaOx stone formation in GHS rats.
背景/目的:高钙尿症是导致草酸钙结石形成的最常见的可识别风险因素。增加口服镁的摄入可能会通过与肠道草酸结合,减少草酸钙结石的形成,从而减少吸收和/或结合尿液中的草酸,降低尿液过饱和度。本研究评估了口服镁对遗传高钙尿结石形成(GHS)大鼠模型中 24 小时尿液离子排泄、过饱和度和肾结石形成的影响,该模型模拟了人类特发性高钙尿症。
当给予草酸前体羟脯氨酸时,每个 GHS 大鼠都会形成草酸钙结石。GHS 大鼠喂食正常钙和磷饮食,同时补充羟脯氨酸以诱导草酸钙形成,然后分为三组,每组 10 只大鼠:对照组喂食含 4.0 g/kg MgO 的饮食、低镁组(0.5 g/kg)和高镁组(8 g/kg)。6 周后,收集 24 小时尿液,测定尿液化学和过饱和度。定量结石形成。
与对照组相比,低镁和高镁组大鼠的尿液镁含量明显减少和增加。饮食镁不改变尿钙排泄,而低镁饮食导致尿草酸显著减少。低镁饮食使尿草酸钙过饱和度显著增加,而高镁饮食使尿草酸钙过饱和度显著降低。在 6 周的治疗期间,饮食镁对结石形成没有影响。
饮食镁可降低 GHS 大鼠的尿液过饱和度,但不能降低草酸钙结石的形成。