Evidence map›Paper›PMID 31071222›Full record

ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2020

Most exposed: the endothelium in chronic kidney disease.

Marc Vila Cuenca, Peter L Hordijk, Marc G Vervloet

Open access · hybridAbstract readReview
In one paragraph

Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026
    Review
  3. Article
  4. International journal of molecular sciences · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Towards a better understanding of arterial calcification disease progression in CKD: investigation of early pathological alterations.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
  18. 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.

Marc Vila CuencaDepartment of Nephrology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, The Netherlands.
Peter L HordijkDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, The Netherlands.
Marc G VervloetDepartment of Nephrology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence indicates that the pathological changes of the endothelium may contribute to the development of cardiovascular complications in chronic kidney disease (CKD). Non-traditional risk factors related to CKD are associated with the incidence of cardiovascular disease, but their role in uraemic endothelial dysfunction has often been disregarded. In this context, soluble α-Klotho and vitamin D are of importance to maintain endothelial integrity, but their concentrations decline in CKD, thereby contributing to the dysfunction of the endothelial lining. These hormonal disturbances are accompanied by an increment of circulating fibroblast growth factor-23 and phosphate, both exacerbating endothelial toxicities. Furthermore, impaired renal function leads to an increment of inflammatory mediators, reactive oxygen species and uraemic toxins that further aggravate the endothelial abnormalities and in turn also inhibit the regeneration of disrupted endothelial lining. Here, we highlight the distinct endothelial alterations mediated by the abovementioned non-traditional risk factors as demonstrated in experimental studies and connect these to pathological changes in CKD patients, which are driven by endothelial disturbances, other than atherosclerosis. In addition, we describe therapeutic strategies that may promote restoration of endothelial abnormalities by modulating imbalanced mineral homoeostasis and attenuate the impact of uraemic retention molecules, inflammatory mediators and reactive oxygen species. A clinical perspective on endothelial dysfunction in CKD may translate into reduced structural and functional abnormalities of the vessel wall in CKD, and ultimately improved cardiovascular disease.

Indexed as

AnimalsEndothelium, VascularHumansRenal Insufficiency, ChronicVascular DiseasescardiovascularCKDendothelial dysfunctionmineral metabolismuraemic toxins

Identifiers

PMID31071222
PMCPMC7473805
OpenAlexW2938642255

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.