Clonal haematopoiesis and cardiovascular-kidney-metabolic syndrome: a cohort study
Authors' conclusion
These findings identify non-DNMT3A CHIP as a marker of CKM progression and support inflammatory mechanisms linking CHIP to CKM syndrome.
Study context
- Population
- UK Biobank participants without a history of hematologic malignancy15,486 (3.4%) had clonal haematopoiesis of indeterminate potential (CHIP)
- Participants
- 451,460 participants
- Exposure
- CHIP vs no CHIP
- CHIPn = 15,486
- Outcome
- CKM stage and progression to stage 4 CKM syndrome
- Follow-up
- Median (IQR) 13.5 (12.6-14.3) years
Methodological detailsUK Biobank, proteomic mediation analysis
- UK Biobank
- Proteomic mediation analysis
Main finding
As reported in the abstract
CKM stage and progression to stage 4 CKM
Each group vs no CHIPEstimate (95% CI)P value
TET2 CHIPhigher CKM stage; FDR-corrected
aOR 1.10(1.00–1.20)
P = 0.045JAK2 CHIPhigher CKM stage; FDR-corrected
aOR 1.68(1.20–2.35)
P = 0.003Non-DNMT3A CHIPprogression to stage 4 CKM; FDR-corrected
aHR 1.24(1.17–1.31)
P < 0.001Observational data: associations, not effects.
Further findings
Proteomic mediators of progression to stage 4 cardiovascular-kidney-metabolic (CKM) in non-DNMT3A CHIP
- Enriched for immune and inflammatory signalling pathways
Original publication
Clonal haematopoiesis and cardiovascular-kidney-metabolic syndrome: a cohort study. Eur Heart J. Published 30 August 2026. doi:10.
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