A Biomarker‐Enhanced Model for Prediction of Acute Kidney Injury and Cardiovascular Risk Following Angiographic Procedures: CASABLANCA AKI Prediction Substudy

Author:

Mohebi Reza12ORCID,van Kimmenade Roland3,McCarthy Cian12,Gaggin Hanna12,Mehran Roxana4ORCID,Dangas George4ORCID,Januzzi James L.125ORCID

Affiliation:

1. Massachusetts General Hospital Boston MA

2. Harvard Medical School Boston MA

3. Cardiology Division Radboud UMC Nijmegen the Netherlands

4. The Zena and Michael A Wiener Cardiovascular InstituteIcahn School of Medicine at Mount Sinai New York NY

5. Baim Institute for Clinical Research Boston MA

Abstract

Background The 2020 Acute Disease Quality Initiative Consensus provided recommendations on novel acute kidney injury biomarkers. In this study, we sought to assess the added value of novel kidney biomarkers to a clinical score in the CASABLANCA (Catheter Sampled Blood Archive in Cardiovascular Diseases) study. Methods and Results We evaluated individuals undergoing coronary and/or peripheral angiography and added 4 candidate biomarkers for acute kidney injury (kidney injury molecule‐1, interleukin‐18, osteopontin, and cystatin C) to a previously described contrast‐associated acute kidney injury (CA‐AKI) risk score. Participants were categorized into integer score groups based on the risk assigned by the biomarker‐enhanced CA‐AKI model. Risk for incident cardiorenal outcomes during a median 3.7 years of follow‐up was assessed. Of 1114 participants studied, 55 (4.94%) developed CA‐AKI. In adjusted models, neither kidney injury molecule‐1 nor interleukin‐18 improved discrimination for CA‐AKI; addition of osteopontin and cystatin C to the CA‐AKI clinical model significantly increased the c‐statistic from 0.69 to 0.73 ( P for change <0.001) and resulted in a Net Reclassification Index of 59.4. Considering those with the lowest CA‐AKI integer score as a reference, the intermediate, high‐risk, and very‐high‐risk groups were associated with adverse cardiorenal outcomes. The corresponding hazard ratios of the very‐high‐risk group were 3.39 (95% CI, 2.14–5.38) for nonprocedural acute kidney injury, 5.58 (95% CI, 3.23–9.63) for incident chronic kidney disease, 6.21 (95% CI, 3.67–10.47) for myocardial infarction, and 8.94 (95% CI, 4.83–16.53) for all‐cause mortality. Conclusions A biomarker‐enhanced risk model significantly improves the prediction of CA‐AKI beyond clinical variables alone and may stratify the risk of future cardiorenal outcomes. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00842868.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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