Evidence map›Paper›PMID 31695023›Full record

ReviewExperimental & molecular medicine2019

Genetic causes of primary aldosteronism.

Eric Seidel, Julia Schewe, Ute I Scholl

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. The Story of Aldosterone Escape.Journal of the American Society of Nephrology : JASN · 2026
    Review
  3. Observational
  4. Article
  5. Article
  6. Clinical value ofEJNMMI research · 2024
    Article
  7. Review
  8. What We Know about and What Is New in Primary Aldosteronism.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Genetics of Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. A Chinese pedigree with glucocorticoid remediable aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    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 1 institution in 1 country.

Eric Seidel *Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Nephrology and Medical Intensive Care, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0003-3334-3950
Julia Schewe *Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Nephrology and Medical Intensive Care, 13353, Berlin, Germany.
Ute I SchollCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Nephrology and Medical Intensive Care, 13353, Berlin, Germany. ute.scholl@charite.de.ORCID http://orcid.org/0000-0002-0309-8045
Humboldt-Universität zu Berlin · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SCHO 1386/2-1Fritz Thyssen Stiftung (Fritz Thyssen Foundation) 10.16.1.027MN
6 · The paper itself

Abstract

Primary aldosteronism is characterized by at least partially autonomous production of the adrenal steroid hormone aldosterone and is the most common cause of secondary hypertension. The most frequent subforms are idiopathic hyperaldosteronism and aldosterone-producing adenoma. Rare causes include unilateral hyperplasia, adrenocortical carcinoma and Mendelian forms (familial hyperaldosteronism). Studies conducted in the last eight years have identified somatic driver mutations in a substantial portion of aldosterone-producing adenomas, including the genes KCNJ5 (encoding inwardly rectifying potassium channel GIRK4), CACNA1D (encoding a subunit of L-type voltage-gated calcium channel Ca

Indexed as

Adrenal Gland DiseasesAnimalsbeta CateninCalcium Channels, L-TypeG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHumansHyperaldosteronismHypertensionSodium-Potassium-Exchanging ATPaseATP1A1 protein, humanbeta CateninCACNA1D protein, humanCalcium Channels, L-TypeCTNNB1 protein, humanG Protein-Coupled Inwardly-Rectifying Potassium ChannelsKCNJ5 protein, humanSodium-Potassium-Exchanging ATPase

Identifiers

PMID31695023
PMCPMC6834635
OpenAlexW2982893294

What OpenQuestion 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 OpenQuestion graph.