Evidence map›Paper›PMID 37612380›Full record

ReviewNature reviews. Nephrology2023

Primary aldosteronism: molecular medicine meets public health.

Elena A B Azizan, William M Drake, Morris J Brown

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Evaluation of Aldosterone Suppression by Cinnarizine, a Putative Cav1.3 Inhibitor.The Journal of clinical endocrinology and metabolism · 2025
    Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Mild autonomous cortisol secretion in primary aldosteronism: the origin of cortisol.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  9. ccfDNA analysis for the classification of adrenocortical adenomas.Journal of endocrinological investigation · 2025
    Article
  10. Multiomics analysis unveils the cellular ecosystem with clinical relevance in aldosterone-producing adenomas withProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. The effect of adrenalectomy on bleomycin-induced pulmonary fibrosis in mice.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  17. Hypertension research 2024 update and perspectives: basic research.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  18. SomaticHypertension (Dallas, Tex. : 1979) · 2024
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Elena A B AzizanDepartment of Medicine, Faculty of Medicine, The National University of Malaysia (UKM), Kuala Lumpur, Malaysia.ORCID 0000-0002-5549-4242
William M DrakeSt Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom.
Morris J BrownEndocrine Hypertension, Department of Clinical Pharmacology and Precision Medicine, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom. morris.brown@qmul.ac.uk.ORCID 0000-0001-8409-1082
Queen Mary University of London · GBSt Bartholomew's Hospital · GB

Funding

British Heart Foundation FS/14/75/31134British Heart Foundation PG/16/40/32137Department of Health 14/145/09Medical Research Council MR/S006869/1
6 · The paper itself

Abstract

Primary aldosteronism is the most common single cause of hypertension and is potentially curable when only one adrenal gland is the culprit. The importance of primary aldosteronism to public health derives from its high prevalence but huge under-diagnosis (estimated to be <1% of all affected individuals), despite the consequences of poor blood pressure control by conventional therapy and enhanced cardiovascular risk. This state of affairs is attributable to the fact that the tools used for diagnosis or treatment are still those that originated in the 1970-1990s. Conversely, molecular discoveries have transformed our understanding of adrenal physiology and pathology. Many molecules and processes associated with constant adrenocortical renewal and interzonal metamorphosis also feature in aldosterone-producing adenomas and aldosterone-producing micronodules. The adrenal gland has one of the most significant rates of non-silent somatic mutations, with frequent selection of those driving autonomous aldosterone production, and distinct clinical presentations and outcomes for most genotypes. The disappearance of aldosterone synthesis and cells from most of the adult human zona glomerulosa is the likely driver of the mutational success that causes aldosterone-producing adenomas, but insights into the pathways that lead to constitutive aldosterone production and cell survival may open up opportunities for novel therapies.

Indexed as

AdenomaHyperaldosteronismAdultAldosteroneHumansMolecular MedicinePublic HealthAldosterone

Identifiers

PMID37612380
PMCPMC7615304
OpenAlexW4386086507

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.