Evidence map›Paper›PMID 25294232›Full record

ReviewJournal of the American Society of Nephrology : JASN2015

Role of the vascular wall in sodium homeostasis and salt sensitivity.

Rik H G Olde Engberink, Nienke M G Rorije, Jaap J Homan van der Heide, Bert-Jan H van den Born, Liffert Vogt

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Review
  8. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. From salt to hypertension, what is missed?Journal of clinical hypertension (Greenwich, Conn.) · 2021
    Review
  17. Article
  18. Review
  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

5 authors at 3 institutions in 2 countries.

Rik H G Olde EngberinkDepartment of Internal Medicine, Divisions of Nephrology, and.
Nienke M G RorijeDepartment of Internal Medicine, Divisions of Nephrology, and.
Jaap J Homan van der HeideDepartment of Internal Medicine, Divisions of Nephrology, and.
Bert-Jan H van den BornDepartment of Internal Medicine, Vascular Medicine, Academic Medical Centre, University of Amsterdam, The Netherlands.
Liffert VogtDepartment of Internal Medicine, Divisions of Nephrology, and l.vogt@amc.uva.nl.
Pediatric Nephrology of Alabama · USAcademic Medical Center · NLUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive sodium intake is associated with both hypertension and an increased risk of cardiovascular events, presumably because of an increase in extracellular volume. The extent to which sodium intake affects extracellular volume and BP varies considerably among individuals, discriminating subjects who are salt-sensitive from those who are salt-resistant. Recent experiments have shown that, other than regulation by the kidney, sodium homeostasis is also regulated by negatively charged glycosaminoglycans in the skin interstitium, where sodium is bound to glycosaminoglycans without commensurate effects on extracellular volume. The endothelial surface layer is a dynamic layer on the luminal side of the endothelium that is in continuous exchange with flowing blood. Because negatively charged glycosaminoglycans are abundantly present in this layer, it may act as an intravascular buffer compartment that allows sodium to be transiently stored. This review focuses on the putative role of the endothelial surface layer as a contributor to salt sensitivity, the consequences of a perturbed endothelial surface layer on sodium homeostasis, and the endothelial surface layer as a possible target for the treatment of hypertension and an expanded extracellular volume.

Indexed as

Water-Electrolyte BalanceAnimalsEndothelium, VascularHumansSodiumSodiumBPcardiovascularendothelial cellsEnNaCsalt sensitivitysodium

Identifiers

PMID25294232
PMCPMC4378110
OpenAlexW2130031503

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.