Evidence map›Paper›PMID 37884787›Full record

ReviewNature reviews. Nephrology2024

Clonal haematopoiesis, ageing and kidney disease.

Caitlyn Vlasschaert, Matthew B Lanktree, Michael J Rauh, Tanika N Kelly, Pradeep Natarajan

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Clonal Hematopoiesis in Kidney Disease.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Clonal Hematopoiesis of Indeterminate Potential and Progression of CKD.Journal of the American Society of Nephrology : JASN · 2025
    Article
  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

5 authors at 5 institutions in 2 countries.

Caitlyn VlasschaertDepartment of Medicine, Queen's University, Kingston, Ontario, Canada.
Matthew B LanktreeDepartment of Medicine and Department of Health Research Methods, Evidence and Impact, McMaster University, Hamilton, Ontario, Canada.ORCID 0000-0002-5750-6286
Michael J RauhDepartment of Pathology and Molecular Medicine, Kingston, Ontario, Canada.ORCID 0000-0002-8346-5537
Tanika N KellyDivision of Nephrology, Department of Medicine, College of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Pradeep NatarajanCardiovascular Research Center and Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. pnatarajan@mgh.harvard.edu.ORCID 0000-0001-8402-7435
Broad Institute · USKingston Health Sciences Centre · CAPopulation Health Research Institute · CAQueen's University · CAUniversity of Illinois Chicago · US

Funding

Clonal hematopoiesis in humans: determinants of development and progressionR01HL148050 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BALLANTYNE, CHRISTIE MITCHELL, NATARAJAN, PRADEEP · 2019 to 2022
$5.9M
CLONAL HEMATOPOIESIS OF INDETERMINATE POTENTIAL IN CHRONIC KIDNEY DISEASE PATIENTSR01DK125782 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KELLY, TANIKA NICOLE · 2021 to 2025
$3.3M
NHLBI NIH HHS R01 HL148050NIDDK NIH HHS R01 DK125782
6 · The paper itself

Abstract

Clonal haematopoiesis of indeterminate potential (CHIP) is a preclinical condition wherein a sizeable proportion of an individual's circulating blood cells are derived from a single mutated haematopoietic stem cell. CHIP occurs frequently with ageing - more than 10% of individuals over 65 years of age are affected - and is associated with an increased risk of disease across several organ systems and premature death. Emerging evidence suggests that CHIP has a role in kidney health, including associations with predisposition to acute kidney injury, impaired recovery from acute kidney injury and kidney function decline, both in the general population and among those with chronic kidney disease. Beyond its direct effect on the kidney, CHIP elevates the susceptibility of individuals to various conditions that can detrimentally affect the kidneys, including cardiovascular disease, obesity and insulin resistance, liver disease, gout, osteoporosis and certain autoimmune diseases. Aberrant pro-inflammatory signalling, telomere attrition and epigenetic ageing are potential causal pathophysiological pathways and mediators that underlie CHIP-related disease risk. Experimental animal models have shown that inhibition of inflammatory cytokine signalling can ameliorate many of the pathological effects of CHIP, and assessment of the efficacy and safety of this class of medications for human CHIP-associated pathology is ongoing.

Indexed as

Acute Kidney InjuryClonal HematopoiesisAgingAnimalsHematopoiesisHematopoietic Stem CellsHumansMutation

Identifiers

PMID37884787
PMCPMC10922936
OpenAlexW4387957963

What OpenQuestion holds

Textmetadata
LicenceTDM
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.