Soluble suppression of tumorigenicity 2 associated with contrast-induced acute kidney injury in patients with STEMI

Abstract

Background

Contrast-induced acute kidney injury (CI-AKI) is a common complication after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI). Soluble suppression of tumorigenicity 2 (sST2) is associated with AKI. However, the relationship between sST2 and CI-AKI is unclear. This study aimed to investigate the relationship between sST2 and CI-AKI in patients with STEMI.

Methods

This was a single-center retrospective observational study. Patients diagnosed with STEMI in the Yichun People’s Hospital from February 2020 to May 2024 were continuously included. CI-AKI was defined as an increase in serum creatinine of at least 50% or 0.3 mg/dL from baseline within 48–72 h after contrast exposure.

Results

The incidence of CI-AKI after PCI was 12.4% (98/791). Univariate analysis showed that age, fasting plasma glucose, diabetes mellitus, Killip class, left ventricular ejection fraction, estimated glomerular filtration rate, high sensitivity troponin T, N-terminal pro-B-type natriuretic peptide, and sST2 were associated with CI-AKI. The above factors were included in a multivariate analysis, which showed that sST2 was an independent factor for CI-AKI after PCI. The restricted cubic splines showed a nonlinear dose–response relationship between sST2 and CI-AKI (P < 0.001). The integration of the sST2 could significantly improve the ability of the model to identify CI-AKI (NRI 0.681, 95% CI 0.474–0.887; IDI 0.063, 95% CI 0.038–0.099).

Conclusion

Elevated sST2 is an independent risk factor for CI-AKI after PCI in patients with STEMI. Integration of sST2 can significantly improve the risk model for CI-AKI.