ReviewNature reviews. Disease primers2026
Primary aldosteronism.
Review in Nature reviews. Disease primers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- From bench to bedside: primary aldosteronism revisited.Endocrine connections · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism (PA) results from excessive aldosterone production by one or both adrenal glands and is an important cause of hypertension, leading to increased cardiovascular and renal morbidities. PA is primarily caused by a spectrum of somatic or germline mutations in aldosterone-driver genes and superimposed aberrant adrenal expression of various G-protein-coupled receptors and their ligands, leading to dysregulated aldosterone production. PA remains underdiagnosed, and simplified testing by measuring renin and aldosterone is recommended in all people with hypertension to maximize the diagnosis of PA. Some individuals with PA may also have co-secretion of cortisol, which contributes to cardiometabolic morbidities. Adrenal vein sampling, emerging functional imaging and novel biomarkers can identify whether a unilateral source of PA can be treated with surgical adrenalectomy. However, the majority of patients with PA have bilateral disease, warranting medical therapy with dietary sodium restriction and mineralocorticoid receptor antagonists, and aldosterone synthase inhibitors in the near future. Medical therapy objectives are to normalize blood pressure and serum potassium; a rise in renin can serve as a biomarker of adequate therapy and reduced risk for adverse cardio-renal outcomes. Patients with PA should be monitored longitudinally for disease progression or recurrence, to manage potential adverse effects of treatment, and to optimize therapy of cardiovascular and other co-morbidities.
Indexed as
Identifiers
42350437What OpenQuestion 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 OpenQuestion graph.