Evidence map›Paper›PMID 31564964›Full record

ArticleIntegrated blood pressure control2019

Liddle's syndrome mechanisms, diagnosis and management.

Benjamin T Enslow, James D Stockand, Jonathan M Berman

Open access · goldAbstract read
In one paragraph

Article in Integrated blood pressure control, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Guideline
  2. Dietary Salt Intake and Hypertension in Chronic Kidney Disease.Electrolyte & blood pressure : E & BP · 2026
    Review
  3. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  4. Failure to thrive in children with tubulopathies.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Correspondence: New-onset hypertension in COVID-19 patients.The British journal of cardiology · 2025
    Article
  11. The roles of the ubiquitin-proteasome system in renal disease.International journal of medical sciences · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023
    Review
  18. Review
  19. Article
  20. Differentiated mouse kidney tubuloids as a novelFrontiers in cell and developmental biology · 2023
    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 1 country.

Benjamin T EnslowUT Health, San Antonio, TX, USA.ORCID 0000-0003-4822-0216
James D StockandUT Health, San Antonio, TX, USA.
Jonathan M BermanNew York Institute of Technology College of Osteopathic Medicine at Arkansas State University, Jonesboro, AR, USA.ORCID 0000-0001-6547-9647
The University of Texas Health Science Center at San Antonio · USArkansas State University · US

Funding

PATHOBIOLOGY OF OCCLUSIVE VASCULAR DISEASET32HL007446 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean Chrisostome Bopassa · 1985 to 2026
$8.9M
San Antonio Biomedical Education and ResearchK12GM111726 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LECHLEITER, JAMES D, OYAJOBI, BABATUNDE OLUKAYODE · 2015 to 2024
$7.6M
Purinergic regulation of ENaC in the distal nephronR01DK113816 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI STOCKAND, JAMES D · 2018 to 2021
$1.4M
Regulation of ENaC by Casein Kinase 2R01DK117909 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI STOCKAND, JAMES D · 2018 to 2021
$1.4M
Defining the Contribution of ENaC to ADH-mediated Water and Sodium ExcretionR01DK103758 · NIDDK · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI PAO, ALAN C, STOCKAND, JAMES D · 2016 to 2019
$1.3M
NHLBI NIH HHS T32 HL007446NIDDK NIH HHS F32 DK115036NIDDK NIH HHS R01 DK103758NIDDK NIH HHS R01 DK113816NIDDK NIH HHS R01 DK117909NIGMS NIH HHS K12 GM111726
6 · The paper itself

Abstract

Liddle's syndrome is a genetic disorder characterized by hypertension with hypokalemic metabolic alkalosis, hyporeninemia and suppressed aldosterone secretion that often appears early in life. It results from inappropriately elevated sodium reabsorption in the distal nephron. Liddle's syndrome is caused by mutations to subunits of the Epithelial Sodium Channel (ENaC). Among other mechanisms, such mutations typically prevent ubiquitination of these subunits, slowing the rate at which they are internalized from the membrane, resulting in an elevation of channel activity. A minority of Liddle's syndrome mutations, though, result in a complementary effect that also elevates activity by increasing the probability that ENaC channels within the membrane are open. Potassium-sparing diuretics such as amiloride and triamterene reduce ENaC activity, and in combination with a reduced sodium diet can restore normotension and electrolyte imbalance in Liddle's syndrome patients and animal models. Liddle's syndrome can be diagnosed clinically by phenotype and confirmed through genetic testing. This review examines the clinical features of Liddle's syndrome, the differential diagnosis of Liddle's syndrome and differentiation from other genetic diseases with similar phenotype, and what is currently known about the population-level prevalence of Liddle's syndrome. This review gives special focus to the molecular mechanisms of Liddle's syndrome.

Indexed as

blood pressuredistal nephronENaChypertensionLiddle’s syndrome

Identifiers

PMID31564964
PMCPMC6731958
OpenAlexW2971537578

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.