ArticleClinical and experimental nephrology2026
The amount of sodium intake may affect the susceptibility to treatment with mineralocorticoid receptor antagonists in patients with primary aldosteronism.
Article in Clinical and experimental nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPatients 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.
methodsA total of 90 patients who received eplerenone or esaxerenone for PA treatment were included in the study. Patients whose PRA was ≥ 1.0 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.
resultsBoth 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.
conclusionAlthough sodium restriction is suggested to facilitate attainment of post-treatment PRA ≥ 1.0 ng/mL/h, a marker of adequate aldosterone blockade, it remains uncertain whether achieving PRA ≥ 1.0 ng/mL/h is associated with favorable renal outcomes.
Indexed as
Identifiers
42126723What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.