High-sensitivity C-reactive protein predicts contrast-induced nephropathy after primary percutaneous coronary

Yong Liu1, Ning Tan, Ying-Ling Zhou

  • 1Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, PR China.

Journal of Nephrology
|September 20, 2011
PubMed

Insights

High-sensitivity C-reactive protein (hs-CRP) levels predict contrast-induced nephropathy (CIN) risk in ST-segment elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI). Elevated hs-CRP significantly indicates higher CIN incidence and in-hospital death risk.

Area of Science:

  • Cardiology
  • Nephrology
  • Biomarkers

Background:

  • Contrast-induced nephropathy (CIN) is a complication following procedures using contrast media.
  • Investigating novel biomarkers for CIN risk prediction is crucial, especially in acute myocardial infarction.
  • High-sensitivity C-reactive protein (hs-CRP) has not been extensively studied as a CIN risk factor.

Purpose of the Study:

  • To evaluate the predictive value of hs-CRP for CIN risk.
  • To assess hs-CRP in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).

Main Methods:

  • Prospective observation of 165 STEMI patients undergoing primary PCI.
  • CIN defined as serum creatinine increase >0.5 mg/dL within 48-72 hours post-contrast.
  • Analysis of hs-CRP quartiles, receiver operator characteristic (ROC) curves, and multivariate logistic regression.

Main Results:

  • CIN occurred in 10% of patients.
  • CIN incidence significantly increased with hs-CRP quartiles (P-trend <0.001).
  • An hs-CRP level of 16.10 mg/L was identified as a discriminator for CIN (OR=6.51, P<0.05) after adjustment.

Conclusions:

  • Elevated hs-CRP (>16.10 mg/L) is a significant and independent predictor of CIN.
  • hs-CRP may aid in identifying high-risk STEMI patients for CIN prevention strategies.
  • This finding highlights the role of inflammation in CIN pathogenesis post-PCI.
Abstract

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