Association between copeptin and contrast-induced nephropathy in patients with ST-elevation myocardial infarction
Ersin Yildirim1, Ayca Turer Cabbar2
1Istanbul Umraniye Education and Research Hospital, University of Health Sciences, Department of Cardiology, Turkey.
Insights
High copeptin levels predict contrast-induced nephropathy (CIN) in ST-elevation myocardial infarction (STEMI) patients. Early detection of high copeptin can guide preventive measures for CIN.
Area of Science:
- Cardiology
- Nephrology
- Biomarkers
Background:
- Contrast-induced nephropathy (CIN) is a complication following procedures using contrast media.
- ST-elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention are at risk for CIN.
Purpose of the Study:
- To evaluate the predictive value of copeptin levels for the development of CIN.
- To identify early indicators for CIN in STEMI patients.
Main Methods:
- A cohort of 274 STEMI patients undergoing primary percutaneous coronary intervention was studied.
- Patients were categorized into CIN-positive (CIN+) and CIN-negative (CIN-) groups.
- Demographic data, laboratory findings, and risk factors were compared between groups.
Main Results:
- Copeptin levels and peak creatinine were significantly higher in the CIN+ group.
- Copeptin level at hospital admission independently predicted CIN development (OR: 2.36, p=0.005).
- Female gender was more prevalent in the CIN- group.
Conclusions:
- Copeptin is a reliable and rapidly detectable independent predictor of CIN in acute STEMI patients.
- Elevated copeptin levels warrant heightened awareness and early initiation of preventive strategies for CIN.
- This finding aids clinicians in risk stratification and timely intervention.
Objective:
The aim of this study was to investigate the predictive value of copeptin levels in the development of contrast-induced nephropathy (CIN).
Methods:
A total of 274 patients diagnosed with ST-elevation myocardial infarction (STEMI) and who had undergone primary percutaneous coronary intervention were included in the study. The patients were divided into two groups according to the presence (CIN+) or absence (CIN-) of CIN. These groups were compared in terms of demographic characteristics, laboratory findings and risk factors.
Results:
Copeptin levels (10.68±6.43 vs. 7.07±05.53 pmol/l; p<0.001) and peak creatinine (1.46±1.20 vs. 1.03±0.20 mg/dl; p=0.005) were significantly higher in the CIN+ group than in the CIN- group. Female gender was significantly more prevalent in the CIN- group compared to the CIN+ group (19% vs. 8.6%; p<0.05). Copeptin level at hospital admission (OR: 2.36, p=0.005) was found to be an independent predictor for CIN development.
Conclusion:
Copeptin level is an independent predictor of CIN development in patients with acute STEMI that can be detected rapidly and easily. This result indicates that physicians should be aware of the possibility of CIN development in patients with high copeptin levels and preventive measures should start early.
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