Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Boston, MA, US.
Division of Endocrinology and Metabolism, Department of Medicine, Duke University, Durham, NC, US.
J Clin Endocrinol Metab. 2020 Jun 1;105(6):1937-46. doi: 10.1210/clinem/dgaa123.
Complex relationships between aldosterone and calcium homeostasis have been proposed.
To disentangle the influence of aldosterone and intravascular volume on calcium physiology.
Patient-oriented and epidemiology studies.
Clinical research center and nationwide cohorts.
PARTICIPANTS/INTERVENTIONS: Patient-oriented study (n = 18): Participants were evaluated after completing a sodium-restricted (RES) diet to contract intravascular volume and after a liberalized-sodium (LIB) diet to expand intravascular volume. Cross-sectional studies (n = 3755): the association between 24h urinary sodium and calcium excretion and risk for kidney stones was assessed.
Patient-oriented study: compared to a RES-diet, a LIB-diet suppressed renin activity (LIB: 0.3 [0.1, 0.4] vs. RES: 3.1 [1.7, 5.3] ng/mL/h; P < 0.001) and plasma aldosterone (LIB: 2.0 [2.0, 2.7] vs. RES: 20.0 [16.1, 31.0] vs. ng/dL; P < 0.001), but increased calciuria (LIB: 238.4 ± 112.3 vs. RES: 112.9 ± 60.8 mg/24hr; P < 0.0001) and decreased serum calcium (LIB: 8.9 ± 0.3 vs. RES: 9.8 ± 0.4 mg/dL; P < 0.0001). Epidemiology study: mean urinary calcium excretion was higher with greater urinary sodium excretion. Compared to a urinary sodium excretion of < 120 mEq/day, a urinary sodium excretion of ≥220 mEq/day was associated with a higher risk for having kidney stones in women (risk ratio = 1.79 [95% confidence interval 1.05, 3.04]) and men (risk ratio = 2.06 [95% confidence interval 1.27, 3.32]).
High dietary sodium intake suppresses aldosterone, decreases serum calcium, and increases calciuria and the risk for developing kidney stones. Our findings help disentangle the influences of volume from aldosterone on calcium homeostasis and provide support for the recommendation to restrict dietary sodium for kidney stone prevention.
醛固酮与钙稳态之间存在复杂的关系。
阐明醛固酮和血管内容量对钙生理学的影响。
面向患者的研究和流行病学研究。
临床研究中心和全国队列。
参与者/干预措施：面向患者的研究（n=18）：参与者在完成限钠（RES）饮食以收缩血管内容量后和在进行自由钠（LIB）饮食以扩张血管内容量后接受评估。横断面研究（n=3755）：评估 24 小时尿钠和钙排泄与肾结石风险之间的关系。
面向患者的研究：与 RES 饮食相比，LIB 饮食抑制了肾素活性（LIB：0.3 [0.1，0.4] vs. RES：3.1 [1.7，5.3] ng/mL/h；P<0.001）和血浆醛固酮（LIB：2.0 [2.0，2.7] vs. RES：20.0 [16.1，31.0] vs. ng/dL；P<0.001），但增加了尿钙排泄（LIB：238.4[112.9，60.8] mg/24 小时；P<0.0001）和降低了血清钙（LIB：8.9[0.9，4] vs. RES：9.8[0.9，0.4] mg/dL；P<0.0001）。流行病学研究：尿钠排泄量越高，尿钙排泄量越高。与尿钠排泄量<120 mEq/天相比，尿钠排泄量≥220 mEq/天与女性（风险比=1.79 [95%置信区间 1.05，3.04]）和男性（风险比=2.06 [95%置信区间 1.27，3.32]）肾结石风险增加相关。
高膳食钠摄入可抑制醛固酮，降低血清钙，增加尿钙排泄量并增加肾结石发病风险。我们的研究结果有助于阐明容量和醛固酮对钙稳态的影响，并为限制膳食钠以预防肾结石提供支持。
