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<p>Primary aldosteronism (PA) is susceptible to cardiovascular and renal damage. However, the role of dietary salt intake in aldosterone-related target organ damage (TOD) in PA remains elusive. This study aimed to investigate whether high salt intake enhances the effect of aldosterone on TOD in PA patients. A total of 361 patients with PA and 102 patients with essential hypertension (EH) were enrolled in this study. All participants underwent tests for the aldosterone/renin ratio, 24-hour urinary sodium, biochemical examination, and TOD assessment via echocardiography, carotid ultrasound, and urine microalbumin measurements. Patients were categorized on the basis of salt intake and aldosterone levels. Compared with the control group, PA patients with high salt intake presented an increased urinary albumin-to-creatinine ratio (UACR), a more significant effect of aldosterone on blood pressure, and remarkable cardiac hypertrophy and renal damage (p &lt; 0.05). Quintile-based regression analysis revealed that the odds ratio between the highest quintile of the plasma aldosterone level and the UACR was twice that of the lowest quintile. In the adjustment models, the relationships between aldosterone and the left ventricular mass index (LVMI) were not statistically significant. Linear correlation analysis further revealed that high salt intake could reinforce the correlation between aldosterone and creatinine, log-UACR and LVMI in PA patients, but this effect was not observed in EH patients. This study suggests that high salt intake can exacerbate aldosterone-related renal impairment, while it is crucial in aldosterone-related cardiac damage in PA patients.</p><p></p>

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High salt intake exacerbates aldosterone-related target organ damage in patients with primary aldosteronism

  • 期刊论文

  • 发表日期：

    2025年7月8日

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  • Xiaona Bu,
  • Fang Sun,
  • Qiang Li,
  • Hexuan Zhang,
  • Nan Jiang,
  • Yushuang Luo,
  • Zhigang Zhao,
  • Zhencheng Yan,
  • Hongbo He,
  • Zhiming Zhu

摘要

Primary aldosteronism (PA) is susceptible to cardiovascular and renal damage. However, the role of dietary salt intake in aldosterone-related target organ damage (TOD) in PA remains elusive. This study aimed to investigate whether high salt intake enhances the effect of aldosterone on TOD in PA patients. A total of 361 patients with PA and 102 patients with essential hypertension (EH) were enrolled in this study. All participants underwent tests for the aldosterone/renin ratio, 24-hour urinary sodium, biochemical examination, and TOD assessment via echocardiography, carotid ultrasound, and urine microalbumin measurements. Patients were categorized on the basis of salt intake and aldosterone levels. Compared with the control group, PA patients with high salt intake presented an increased urinary albumin-to-creatinine ratio (UACR), a more significant effect of aldosterone on blood pressure, and remarkable cardiac hypertrophy and renal damage (p < 0.05). Quintile-based regression analysis revealed that the odds ratio between the highest quintile of the plasma aldosterone level and the UACR was twice that of the lowest quintile. In the adjustment models, the relationships between aldosterone and the left ventricular mass index (LVMI) were not statistically significant. Linear correlation analysis further revealed that high salt intake could reinforce the correlation between aldosterone and creatinine, log-UACR and LVMI in PA patients, but this effect was not observed in EH patients. This study suggests that high salt intake can exacerbate aldosterone-related renal impairment, while it is crucial in aldosterone-related cardiac damage in PA patients.