Evidence map›Paper›PMID 33758363›Full record

ReviewNature reviews. Nephrology2021

Uraemic solutes as therapeutic targets in CKD-associated cardiovascular disease.

Jonathan D Ravid, Mohamed Hassan Kamel, Vipul C Chitalia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 3 pooled it
10.3field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Gut-kidney axis: Dysbiosis and renal disease.World journal of nephrology · 2026
    Review
  5. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Untargeted metabolomics unveils metabolic biomarkers in HFpEF.Frontiers in molecular biosciences · 2025
    Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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.

Jonathan D RavidSchool of Medicine, Boston University School of Medicine, Boston, MA, USA.
Mohamed Hassan KamelRenal Section, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Vipul C ChitaliaRenal Section, Department of Medicine, Boston University School of Medicine, Boston, MA, USA. vichital@bu.edu.ORCID http://orcid.org/0000-0002-6663-6058
Boston University · US

Funding

Thrombotic complication of uremia: role of prothrombotic uremic solutesR01HL132325 · NHLBI · BOSTON MEDICAL CENTER · PI CHITALIA, VIPUL C · 2016 to 2019
$1.7M
Role of intravascular ultrasound in Central Venous Stenosis in ESRD patientsR21DK119740 · NIDDK · BOSTON MEDICAL CENTER · PI CHITALIA, VIPUL C · 2020 to 2021
$503k
NHLBI NIH HHS R01 HL132325NIDDK NIH HHS R21 DK119740
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is characterized by the retention of a myriad of solutes termed uraemic (or uremic) toxins, which inflict damage to several organs, including the cardiovascular system. Uraemic toxins can induce hallmarks of cardiovascular disease (CVD), such as atherothrombosis, heart failure, dysrhythmias, vessel calcification and dysregulated angiogenesis. CVD is an important driver of mortality in patients with CKD; however, reliance on conventional approaches to managing CVD risk is insufficient in these patients, underscoring a need to target risk factors that are specific to CKD. Mounting evidence suggests that targeting uraemic toxins and/or pathways induced by uraemic toxins, including tryptophan metabolites and trimethylamine N-oxide (TMAO), can lower the risk of CVD in patients with CKD. Although tangible therapies resulting from our growing knowledge of uraemic toxicity are yet to materialize, a number of pharmacological and non-pharmacological approaches have the potential to abrogate the effects of uraemic toxins, for example, by decreasing the production of uraemic toxins, by modifying metabolic pathways induced by uraemic toxins such as those controlled by aryl hydrocarbon receptor signalling and by augmenting the clearance of uraemic toxins.

Indexed as

AnimalsCardiovascular DiseasesHumansRenal Insufficiency, ChronicUremia

Identifiers

PMID33758363
OpenAlexW3136544732

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.