Evidence map›Paper›PMID 30124805›Full record

ReviewEndocrine reviews2018

The Expanding Spectrum of Primary Aldosteronism: Implications for Diagnosis, Pathogenesis, and Treatment.

Anand Vaidya, Paolo Mulatero, Rene Baudrand, Gail K Adler

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 2 pooled it
14.3field-weighted citation impact, top 1% of its field
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

142 citing papers in PubMed, 2 syntheses or guidelines pooled it, 276 citations in OpenAlex.

  1. Pooled it
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  11. Primary aldosteronism.Nature reviews. Disease primers · 2026
    Review
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82 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 3 countries.

Anand VaidyaCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Paolo MulateroDivision of Internal Medicine and Hypertension, Department of Medical Sciences, University of Torino, Torino, Italy.
Rene BaudrandProgram for Adrenal Disorders and Hypertension, Department of Endocrinology, Pontificia Universidad Catolica de Chile, Santiago, Chile.
Gail K AdlerCenter for Adrenal Disorders, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · USPontificia Universidad Católica de Chile · CLUniversity of Turin · IT

Funding

TRAINING PROGRAM IN HYPERTENSIONT32HL007609 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 1985 to 2022
$10.2M
Aldosterone and Diabetic Cardiovascular Disease: Research and Mentoring ProgamK24HL103845 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 2011 to 2021
$1.6M
NHLBI NIH HHS K24 HL103845NHLBI NIH HHS T32 HL007609
6 · The paper itself

Abstract

Primary aldosteronism is characterized by aldosterone secretion that is independent of renin and angiotensin II and sodium status. The deleterious effects of primary aldosteronism are mediated by excessive activation of the mineralocorticoid receptor that results in the well-known consequences of volume expansion, hypertension, hypokalemia, and metabolic alkalosis, but it also increases the risk for cardiovascular and kidney disease, as well as death. For decades, the approaches to defining, diagnosing, and treating primary aldosteronism have been relatively constant and generally focused on detecting and treating the more severe presentations of the disease. However, emerging evidence suggests that the prevalence of primary aldosteronism is much greater than previously recognized, and that milder and nonclassical forms of renin-independent aldosterone secretion that impart heightened cardiovascular risk may be common. Public health efforts to prevent aldosterone-mediated end-organ disease will require improved capabilities to diagnose all forms of primary aldosteronism while optimizing the treatment approaches such that the excess risk for cardiovascular and kidney disease is adequately mitigated. In this review, we present a physiologic approach to considering the diagnosis, pathogenesis, and treatment of primary aldosteronism. We review evidence suggesting that primary aldosteronism manifests across a wide spectrum of severity, ranging from mild to overt, that correlates with cardiovascular risk. Furthermore, we review emerging evidence from genetic studies that begin to provide a theoretical explanation for the pathogenesis of primary aldosteronism and a link to its phenotypic severity spectrum and prevalence. Finally, we review human studies that provide insights into the optimal approach toward the treatment of primary aldosteronism.

Indexed as

HyperaldosteronismHumans

Identifiers

PMID30124805
PMCPMC6260247
OpenAlexW2887931962

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.