Incident heart failure in chronic kidney disease: proteomics informs biology and risk stratification
Authors' conclusion
Large-scale proteomics reveal novel circulating protein biomarkers and potential mediators of HF in CKD. Proteomic risk models improve upon the PCP-HF risk score in this population.
Study context
- Population
- Participants with Chronic Kidney Disease (CKD) in the Chronic Renal Insufficiency Cohort (CRIC); SomaScan V4.0 (4638 proteins)CRIC
- Participants
- 2,906 participants
- Exposure
- 48-protein risk model vs PCP-HF risk score
- Outcome
- Incident HF (390 events)
- Follow-up
- 14 years
Methodological detailsproteomic analysis, external validation in Atherosclerosis Risk in Communities (ARIC), Mendelian randomization
- Proteomic analysis
- External validation in ARIC
- Mendelian randomization
Main finding
As reported in the abstract
Discrimination for 14-year incident HF (C-statistic), CRIC
48-protein model
0.790
C-statistic · 95% CI 0.735–0.844
PCP-HF
0.703
C-statistic · 95% CI 0.644–0.762
P = 0.001
Observational data: associations, not effects.
Secondary outcomes
| Outcome | Values |
|---|---|
| C-statistic for incident HF, external validation in ARICValidation cohort (ARIC) | Protein model C-statistic 0.747 (95% CI 0.707–0.787) |
Proteins associated with incident heart failure (HF)
- Proteins associated with incident HF after eGFR adjustment (P < 1 × 10-5)
- Over 200
- Proteins still associated after adjustment incl. NT-proBNP (P < 1 × 10-5)
- 17
- Proteins with Mendelian randomization associations
- six
- Druggable targets among them: FCG2B, IGFBP3, CAH6, ASGR1
- four
Original publication
Incident heart failure in chronic kidney disease: proteomics informs biology and risk stratification. Eur Heart J. Published 17 May 2024. doi:10.
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