Evidence map›Paper›PMID 39660429›Full record

ArticleHypertension (Dallas, Tex. : 1979)2025

Characterizing the Origins of Primary Aldosteronism.

Jenifer M Brown, Brooke Honzel, Laura C Tsai, Julia Milks, Yvonne M Neibuhr, Andrew J Newman, Michael Cherney, David G Stouffer, Richard J Auchus, Anand Vaidya

Abstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Primary aldosteronism.Nature reviews. Disease primers · 2026
    Review
  3. Article
  4. Hypertensive Disorders of Pregnancy and Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2026
    Article
  5. Is It Time to Retire Aldosterone Suppression Testing?American journal of hypertension · 2026
    Review
  6. Article
  7. Hypertensive Disorders of Pregnancy and Primary Aldosteronism.medRxiv : the preprint server for health sciences · 2026
    Article
  8. Article
  9. Subclinical primary aldosteronism.Archives of endocrinology and metabolism · 2025
    Review
  10. Review
  11. Observational
  12. Review
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Jenifer M BrownCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).ORCID 0000-0002-6647-639X
Brooke HonzelCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).ORCID 0009-0005-2824-903X
Laura C TsaiCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).
Julia MilksCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).
Yvonne M NeibuhrCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).
Andrew J NewmanCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).ORCID 0000-0002-8326-1964
Michael CherneyDepartments of Pharmacology and Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor (M.C., D.G.S., R.J.A.).
David G StoufferDepartments of Pharmacology and Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor (M.C., D.G.S., R.J.A.).
Richard J AuchusDepartments of Pharmacology and Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor (M.C., D.G.S., R.J.A.).ORCID 0000-0001-6815-6181
Anand VaidyaCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension (J.M.B., B.H., L.C.T., J.M., Y.M.N., A.J.N., A.V.).ORCID 0000-0002-0314-9252

Funding

TRAINING PROGRAM IN HYPERTENSIONT32HL007609 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 1985 to 2022
$10.2M
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
Adrenal Origins of Aldosterone ExcessR01DK106618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI William E Rainey, Aaron Mark Udager · 2016 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-American Stroke Association 852429NHLBI NIH HHS K23 HL159279NHLBI NIH HHS R01 HL153004NHLBI NIH HHS R01 HL155834NHLBI NIH HHS T32 HL007609NIDDK NIH HHS R01 DK106618NIDDK NIH HHS R01 DK115392
6 · The paper itself

Abstract

backgroundRenin-independent aldosterone production in normotensive people increases risk for developing hypertension. In parallel, normotensive adrenal glands frequently harbor aldosterone-producing micronodules with pathogenic somatic mutations known to induce primary aldosteronism (PA). A deeper understanding of these phenomena would inform the origins of PA and its role in hypertension pathogenesis.

methodsProspectively recruited normotensives underwent detailed characterization of PA features via the following: oral sodium suppression test to evaluate renin-independent aldosterone production, dexamethasone suppression and adrenocorticotropic hormone-stimulation tests to evaluate adrenocorticotropic hormone-mediated aldosterone production, and 24-hour ambulatory blood pressure monitoring. The magnitude of renin-independent aldosterone production was defined via tertiles of 24-hour urinary aldosterone production during the oral sodium suppression test to create unbiased categorizations of the magnitude of PA. Serum aldosterone, serum 18-hybrid steroids, urine tetrahydroaldosterone (biomarkers of aldosterone synthase activity), urinary potassium, and blood pressure (biomarkers of mineralocorticoid receptor activation) were evaluated across tertiles.

resultsThere was a spectrum of autonomous, nonsuppressible, and renin-independent production of aldosterone, 18-hybrid steroids, and 24-hour urinary tetrahydroaldosterone (

conclusionsThe pathophysiologic continuum of PA, characterized by renin-independent and adrenocorticotropic hormone-mediated aldosterone production, and enhanced aldosterone synthase and mineralocorticoid receptor activity, is evident in normotensive people. These findings provide mechanistic explanations to implicate PA in the pathogenesis of a substantial proportion of hypertension.

Indexed as

AldosteroneHyperaldosteronismHypertensionAdrenal GlandsAdrenocorticotropic HormoneAdultBlood PressureBlood Pressure Monitoring, AmbulatoryFemaleHumansMaleMiddle AgedProspective StudiesReninAdrenocorticotropic HormoneAldosteroneReninaldosteroneblood pressurehypertensionprimary aldosteronismrenin

Identifiers

PMID39660429
PMCPMC11735322

What Socratic holds

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Registered trials

None linked

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.