Evidence map›Paper›PMID 25287433›Full record

ReviewNature reviews. Nephrology2014

Chronic kidney disease and premature ageing.

Jeroen P Kooman, Peter Kotanko, Annemie M W J Schols, Paul G Shiels, Peter Stenvinkel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed, 1 pooled it
10.6field-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

227 citing papers in PubMed, 1 synthesis or guideline pooled it, 371 citations in OpenAlex.

  1. Pooled it
  2. High-flux hemodialysis with polymethylmethacrylate membranes reduces soluble CD40L, a mediator of cardiovascular disease in uremia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Trial
  3. Trial
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  5. Trial
  6. Trial
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  14. Clonal Hematopoiesis in Kidney Disease.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

167 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

5 authors at 1 institution in 1 country.

Jeroen P KoomanDepartment of Internal Medicine, Division of Nephrology, Maastricht University Medical Center, PO Box 5800, 6202 AZ Maastrich, Netherlands.
Peter KotankoRenal Research Institute, 315 East 62nd Street, 4th floor, NY 10065, New York, USA.
Annemie M W J ScholsDepartment of Respiratory Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, PO Box 5800, 6202 AZ Maastrich, Netherlands.
Paul G ShielsInstitute of Cancer Sciences, Wolfson Wohl Translational Research Centre, University of Glasgow, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1QH, UK.
Peter StenvinkelDivision of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska University Hospital, Huddinge, Karolinska Institutet, SE-14157 Stockholm, Sweden.
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) shares many phenotypic similarities with other chronic diseases, including heart failure, chronic obstructive pulmonary disease, HIV infection and rheumatoid arthritis. The most apparent similarity is premature ageing, involving accelerated vascular disease and muscle wasting. We propose that in addition to a sedentary lifestyle and psychosocial and socioeconomic determinants, four major disease-induced mechanisms underlie premature ageing in CKD: an increase in allostatic load, activation of the 'stress resistance response', activation of age-promoting mechanisms and impairment of anti-ageing pathways. The most effective current interventions to modulate premature ageing-treatment of the underlying disease, optimal nutrition, correction of the internal environment and exercise training-reduce systemic inflammation and oxidative stress and induce muscle anabolism. Deeper mechanistic insight into the phenomena of premature ageing as well as early diagnosis of CKD might improve the application and efficacy of these interventions and provide novel leads to combat muscle wasting and vascular impairment in chronic diseases.

Indexed as

Risk Reduction BehaviorAgingAging, PrematureEarly DiagnosisFemaleGenetic MarkersHumansImmunity, InnateInflammationMaleMuscular AtrophyOxidative StressPrognosisRenal Insufficiency, ChronicRisk AssessmentSeverity of Illness IndexGenetic Markers

Identifiers

PMID25287433
OpenAlexW1989273717

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.