Evidence map›Paper›PMID 40036317›Full record

Observational studyThe Journal of clinical endocrinology and metabolism2025

Subclinical Primary Aldosteronism Is Characterized by Maladaptive Natriuretic Peptide and Adrenal Hormonal Physiology.

Stéfanie Parisien-La Salle, Jenifer M Brown, Sanan Mahrokhian, Isabelle Hanna, Brooke Honzel, Laura C Tsai, Andrew J Newman, Thomas J Wang, Anand Vaidya

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Primary aldosteronism.Nature reviews. Disease primers · 2026
    Review
  2. Hypertensive Disorders of Pregnancy and Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2026
    Article
  3. Article
  4. Hypertensive Disorders of Pregnancy and Primary Aldosteronism.medRxiv : the preprint server for health sciences · 2026
    Article
  5. Article
  6. Subclinical primary aldosteronism.Archives of endocrinology and metabolism · 2025
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Stéfanie Parisien-La SalleCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Jenifer M BrownCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Sanan MahrokhianCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Isabelle HannaCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Brooke HonzelCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Laura C TsaiCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Andrew J NewmanCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Thomas J WangDepartment of Internal Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Anand VaidyaCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-0314-9252

Funding

Unrecognized Primary Aldosteronism as a Pathogenic Mechanism for Chronic Kidney Disease in DiabetesR01DK115392 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Anand Vaidya · 2018 to 2026
$6.0M
Aldosterone, the Mineralocorticoid Receptor, and Cardiovascular Disease in ObesityR01HL153004 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, ANAND · 2020 to 2024
$4.4M
Primary Aldosteronism Subtypes: Pathophysiology and Steroid SignaturesR01HL155834 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TURCU, ADINA F · 2021 to 2025
$3.5M
Cardiac Perfusion, Structure, and Function across the Primary Aldosteronism SpectrumK23HL159279 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Jenifer Michelle Brown · 2022 to 2026
$1.0M
American Heart Association Career Development Award #852429National Institutes of Health/National Heart, Lung, and Blood Institute T32HL007609NHLBI NIH HHS K23 HL159279NHLBI NIH HHS R01 HL153004NIDDK NIH HHS R01 DK115392NIH HHS R01DK115392NIH HHS R01DK16618NIH HHS R01HL153004NIH HHS R01HL155834
6 · The paper itself

Abstract

contextA continuum of non-suppressible aldosterone production has been demonstrated in normotensive individuals, termed subclinical primary aldosteronism (PA), and is consistently associated with increased risk for developing hypertension and cardiovascular disease. The hormonal mechanisms accounting for subclinical PA are not well understood.

methodsTo quantify the magnitude of subclinical PA, prospectively recruited normotensive participants (n = 75) had their maximally suppressed plasma aldosterone assessed after maintaining supine posture following an oral sodium loading protocol. To investigate the endocrine mechanisms involved with this continuum, multiple maneuvers were conducted to evaluate: (i) natriuretic peptide physiology (N-terminal pro B-type natriuretic peptide [NT-proBNP] suppression and stimulation using dietary sodium modulation); (ii) angiotensin II (AngII)-dependent aldosterone production (via dietary sodium restriction and via infusion of exogenous AngII); (iii) AngII-independent aldosterone production (via saline suppression test [SST]); and (iv) ACTH-mediated aldosterone production (via dexamethasone suppression test and ACTH-stimulation test).

resultsGreater magnitude of subclinical PA was associated with lower basal NT-proBNP (P-trend < .01) and blunted stimulation of NT-proBNP following sodium loading (P-trend = .023). The magnitude of subclinical PA was also associated with greater AngII-dependent (P-trend < .001) and AngII-independent (P-trend < .001) aldosterone production and paralleled the severity of ACTH-mediated aldosterone production (P-trends < .001). Following SST, 24.2% of participants had a post-saline aldosterone greater than 10 ng/dL and 72.7% had a post-saline aldosterone greater than 6 ng/dL, confirming that the continuum of subclinical PA included overt PA pathophysiology within these normotensive participants.

conclusionThese findings demonstrate that the pathophysiologic continuum of subclinical PA in normotensive people is characterized by natriuretic peptide insufficiency and heightened aldosterone responses to both AngII and ACTH. These early maladaptive hormonal changes provide mechanistic explanations for the role of subclinical PA in the pathogenesis of hypertension.

Indexed as

Adrenocorticotropic HormoneAldosteroneAngiotensin IIHyperaldosteronismNatriuretic Peptide, BrainAdrenal GlandsAdultAgedAsymptomatic DiseasesBlood PressureDexamethasoneDiagnostic Techniques, EndocrineDiet, Sodium-RestrictedFemaleHumansLongitudinal StudiesAdrenocorticotropic HormoneAldosteroneAngiotensin IIDexamethasoneNatriuretic Peptide, BrainPeptide Fragmentspro-brain natriuretic peptide (1-76)Sodium, DietaryACTHaldosteroneAngiotensin IINT-proBNPprimary aldosteronism

Identifiers

PMID40036317
PMCPMC12527462

What OpenQuestion holds

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Registered trials

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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.