ReviewAmerican journal of hypertension2026
Is It Time to Retire Aldosterone Suppression Testing?
Review in American journal of hypertension, 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.
- NT-proBNP and its association with autonomous aldosterone production in primary aldosteronism.Therapeutic advances in endocrinology and metabolism · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism (PA) is the most common endocrine hypertension. For decades, PA diagnosis has required proving nonsuppressibility of aldosterone following maneuvers modulating the renin-angiotensin-aldosterone pathway. This includes oral salt suppression, intravenous saline suppression, captopril suppression, and others. Grounded in rational first principles from pathophysiologic considerations and small, early pathophysiologic studies following Conn's initial PA description, such testing has been widely recommended. However, a modern understanding of PA pathophysiology and critical appraisal of diagnostic test studies suggest that traditional suppression testing is not suited to diagnosis or disease definition. There are four main problems recently raised regarding aldosterone suppression testing: (i) PA is now known to exist along a continuous biochemical spectrum and it is scientifically impossible to draw a single, diagnostic threshold within this continuum. (ii) Aldosterone assay uncertainty is sufficiently large to yield contradictory final diagnoses when applied to a threshold during suppression testing. (iii) The pathophysiology of PA is multifactorial with multiple mechanisms not necessarily relevant to salt and volume loading tests. (iv) Finally, meta-analysis of suppression testing studies demonstrated extensive biases and confounders, which have overestimated the diagnostic value. A recent prospective, blinded study of saline suppression for PA diagnosis defined by medical or surgical response to PA-targeted therapy showed no discrimination according to nadir aldosterone level. Given the clinical value of a PA diagnosis and the high prevalence of the disease, modern evidence suggests that aldosterone suppression testing should now be retired from the diagnostic pathway; new ways of approaching the definition of PA are provided to spur further discussion.
Indexed as
Identifiers
What 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.