Background <p>Patients with primary aldosteronism (PA) have an increased risk of developing cardiovascular disease. In patients with bilateral adrenal aldosterone hypersecretion, mineralocorticoid receptor antagonists (MRAs) are recommended; however, the benefit of these agents is observed only in cases that show a sufficient increase in post-treatment PRA (responders). Because renin secretion can be influenced by sodium intake, the increase in post-treatment PRA may be attributable to sodium restriction.</p> Methods <p>A total of 90 patients who received eplerenone or esaxerenone for PA treatment were included in the study. Patients whose PRA was ≥ 1.0&#xa0;ng/mL/h at one year after the initiation of MRAs treatment were defined as responders. The predictors of responders and the effect of sodium intake were investigated.</p> Results <p>Both baseline and post-treatment PRA and PAC levels were higher in responders. In addition, baseline estimated sodium intake tended to be lower, and post-treatment estimated sodium intake was significantly lower in responders. The post-treatment PRA value was significantly correlated with the post-treatment estimated sodium intake, and the post-treatment estimated sodium intake was an independent predictor of responders, suggesting that post-treatment PRA elevation may be partially attributable to adequate sodium restriction. However, the change in the estimated glomerular filtration rate over the 3-year follow-up period was not different between responders and non-responders.</p> Conclusion <p>Although sodium restriction is suggested to facilitate attainment of post-treatment PRA ≥ 1.0&#xa0;ng/mL/h, a marker of adequate aldosterone blockade, it remains uncertain whether achieving PRA ≥ 1.0&#xa0;ng/mL/h is associated with favorable renal outcomes.</p>