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Soluble Suppression of Tumorigenicity 2 Associated with Contrast-induced Acute Kidney Injury in Patients with STEMI

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Publisher Springer
Specialty Nephrology
Date 2024 Sep 12
PMID 39264493
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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.

Citing Articles

Associations between serum 25-hydroxyvitamin D and prognosis of chronic kidney disease: a prospective cohort study.

Mai Y, Yi Y, Wen Y, Huang P, Wang Y, Wang Z Int Urol Nephrol. 2024; 56(10):3323-3334.

PMID: 38767811 DOI: 10.1007/s11255-024-04083-9.

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