Evidence map›Paper›PMID 40147025›Full record

ArticleClinical and translational medicine2025

Sendotypes predict worsening renal function in chronic kidney disease patients.

Thomas McLarnon, Steven Watterson, Sean McCallion, Eamonn Cooper, Andrew R English, Ying Kuan, David S Gibson, Elaine K Murray, Frank McCarroll, Shu-Dong Zhang and 2 more

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  4. 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

12 authors.

Thomas McLarnonSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Steven WattersonSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Sean McCallionSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Eamonn CooperSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Andrew R EnglishSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Ying KuanWestern Health and Social Care Trust, Altnagelvin Area Hospital, Londonderry, UK.
David S GibsonSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Elaine K MurraySchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Frank McCarrollWestern Health and Social Care Trust, Altnagelvin Area Hospital, Londonderry, UK.
Shu-Dong ZhangSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Anthony J BjoursonSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.
Taranjit Singh RaiSchool of Medicine, Personalised Medicine Centre, Ulster University, Londonderry, UK.ORCID 0000-0002-7276-7492

Funding

EU Regional Development Fund Sustainable Competitiveness Program for NINI Public Health AgencyPHA/HSC R&D Division COM/5618/20Western Health & Social Care Trust
6 · The paper itself

Abstract

backgroundSenescence associated secretory phenotype (SASP) contributes to age-related pathology, however the role of SASP in Chronic Kidney Disease (CKD) is unclear. Here, we employ a variety of omic techniques to show that senescence signatures can separate CKD patients into distinct senescence endotypes (Sendotype).

methodsUsing specific numbers of senescent proteins, we clustered CKD patients into two distinct sendotypes based on proteomic expression. These clusters were evaluated with three independent criteria assessing inter and intra cluster distances. Differential expression analysis was then performed to investigate differing proteomic expression between sendotypes.

resultsThese clusters accurately stratified CKD patients, with patients in each sendotype having different clinical profiles. Higher expression of these proteins correlated with worsened disease symptomologies. Biological signalling pathways such as TNF, Janus kinase-signal transducers and activators of transcription (JAK-STAT) and NFKB were differentially enriched between patient sendotypes, suggesting potential mechanisms driving the endotype of CKD.

conclusionOur work reveals that, combining clinical features with SASP signatures from CKD patients may help predict whether a patient will have worsening or stable renal trajectory. This has implications for the CKD clinical care pathway and will help clinicians stratify CKD patients accurately. KEY POINTS: Senescent proteins are upregulated in severe patients compared to mild patients Senescent proteins can stratify patients based on disease severity High expression of senescent proteins correlates with worsening renal trajectories.

Indexed as

Cellular SenescenceRenal Insufficiency, ChronicAdultAgedDisease ProgressionFemaleHumansMaleMiddle AgedPhenotypeProteomicsbiomarkerCKDmachine learningsendotypesenescence

Identifiers

PMID40147025
PMCPMC11949504

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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.