Evidence map›Paper›PMID 19279127›Full record

ArticleAmerican journal of physiology. Renal physiology2009

Urinary endothelin-1 in chronic kidney disease and as a marker of disease activity in lupus nephritis.

Neeraj Dhaun, Pajaree Lilitkarntakul, Iain M Macintyre, Eline Muilwijk, Neil R Johnston, David C Kluth, David J Webb, Jane Goddard

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Endothelin-A receptor antagonism modifies cardiovascular risk factors in CKD.Journal of the American Society of Nephrology : JASN · 2013
    Trial
  3. Review
  4. Sodium intake and biological sex influence urinary endothelin-1 in salt-resistant adults: a pilot study.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  5. Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Mitigation of Cardiovascular Disease and Toxicity through NRF2 Signalling.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Autoimmune-mediated renal disease and hypertension.Clinical science (London, England : 1979) · 2021
    Review
  15. Review
  16. Evaluation of Urinary Big Endothelin-1 in Feline Spontaneous CKD.Animals : an open access journal from MDPI · 2020
    Article
  17. Frontiers in physiology · 2020
    Article
  18. Urinary biomarkers in lupus nephritis.Journal of translational autoimmunity · 2020
    Review
  19. Review
  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

8 authors at 1 institution in 1 country.

Neeraj DhaunThe Queen's Medical Research Institute, 3rd Floor East, Rm. E3.23, 47 Little France Crescent, Edinburgh, EH16 4TJ, United Kingdom. bean.dhaun@ed.ac.uk
Pajaree Lilitkarntakul
Iain M Macintyre
Eline Muilwijk
Neil R Johnston
David C Kluth
David J Webb
Jane Goddard
The Queen's Medical Research Institute · GB

Funding

British Heart Foundation
6 · The paper itself

Abstract

Chronic inflammation contributes to the development and progression of chronic kidney disease (CKD). Identifying renal inflammation early is important. There are currently no specific markers of renal inflammation. Endothelin-1 (ET-1) is implicated in the pathogenesis of CKD. Thus, we investigated the impact of progressive renal dysfunction and renal inflammation on plasma and urinary ET-1 concentrations. In a prospective study, plasma and urinary ET-1 were measured in 132 subjects with CKD stages 1 to 5, and fractional excretion of ET-1 (FeET-1) was calculated. FeET-1, serum C-reactive protein (CRP), urinary ET-1:creatinine ratio, and urinary albumin:creatinine ratio were also measured in 29 healthy volunteers, 85 subjects with different degrees of inflammatory renal disease but normal renal function, and in 10 subjects with rheumatoid arthritis without renal involvement (RA). In subjects with nephritis associated with systemic lupus erythematosus (SLE), measurements were done before and after 6 mo of treatment. In subjects with CKD, plasma ET-1 increased linearly as renal function declined, whereas FeET-1 rose exponentially. In subjects with normal renal function, FeET-1 and urinary ET-1:creatinine ratio were higher in SLE subjects than in other groups (7.7 +/- 2.7%, 10.0 +/- 3.0 pg/mumol, both P < 0.001), and correlated with CRP, and significantly higher than in RA subjects (both P < 0.01) with similar CRP concentrations. In SLE patients, following treatment, FeET-1 fell to 3.6 +/- 1.4% (P < 0.01). Renal ET-1 production increases as renal function declines. In subjects with SLE, urinary ET-1 may be a useful measure of renal inflammatory disease activity while measured renal function is still normal.

Indexed as

AdultAgedBiomarkersEndothelin-1FemaleHumansInflammationKidney Failure, ChronicLupus NephritisMaleMiddle AgedYoung AdultBiomarkersEndothelin-1

Identifiers

PMID19279127
PMCPMC2692450
OpenAlexW2138798549

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.