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Acute kidney injury after primary angioplasty: is contrast-induced nephropathy the culprit?

Session Best Posters session 1

Speaker Oren Caspi

Event : ESC Congress 2015

  • Topic : interventional cardiology and cardiovascular surgery
  • Sub-topic : Coronary Intervention: Complications
  • Session type : Best ePosters

Authors : O Caspi (Haifa,IL), M Habib (Haifa,IL), M Kapeliovich (Haifa,IL), W Markiewicz (Haifa,IL), H Hammerman (Haifa,IL), A Rougin (Haifa,IL), R Beyar (Haifa,IL), D Aronson (Haifa,IL)

Authors:
O. Caspi1 , M. Habib1 , M. Kapeliovich1 , W. Markiewicz1 , H. Hammerman1 , A. Rougin1 , R. Beyar1 , D. Aronson1 , 1Rambam Health Care Campus, Cardiology - Haifa - Israel ,

Citation:
European Heart Journal ( 2015 ) 36 ( Abstract Supplement ), 39

Background: Acute kidney injury (AKI) following primary PCI (PPCI) is frequently interpreted as contrast-induced nephropathy (CIN). However, AKI after PPCI may be the result of other contributing factors including hemodynamic alterations, neurohormonal activation and initiation of drugs that affects renal function.

Purpose: To better isolate the effects of the contrast media exposure in the setting of ST-elevation myocardial infarction (STEMI), we compared the incidence and clinical predictors of AKI in patients (pts) undergoing primary PCI to STEMI pts who were not exposed to contrast media.

Methods: We studied 893 pts with STEMI who underwent PPCI and 973 control pts consisting of those receiving fibrinolysis or pts who were not reperfused, and excluding pts who underwent coronary angiography or PCI other than primary PCI within 72-h from admission. Creatinine levels were obtained on admission and at 24-h, 48-h, 72-h. AKI was defined as creatinine elevations of ≥25% mg/dl or >0.5 mg/dl above baseline at 72-h. Logistic regression was used to identify independent predictors of AKI.

Results: AKI occurred in 146 (16.3% (of PPCI patient and in 157 (16.1%) of the control group (P=0.90). The table shows independent predictors of AKI in the PPCI cohort. Contrast media was a weak predictor of AKI as compared with age, baseline renal dysfunction and hemodynamic compromise. The area under the ROC curve for the model presented in the table was 0.77±0.02, indicating good discrimination. The area under the ROC curve was not altered after excluding contrast amount from the model (0.76). The same model was validated in the control group of patients not exposed to contrast media

Conclusions: In pts with STEMI, age, baseline renal dysfunction and hemodynamic compromise are the main predictors of AKI. Importantly, STEMI pts who were not exposed to contrast media have similar AKI risk as pts undergoing PPCI.

Independent predictors of AKI (PPCI gr.)
VariableOdds Ratio (95% CI)P value
Age (per 10 years)1.28 (1.08–1.52)0.0005
eGFR (per 10 ml/min decrease)1.49 (1.36–1.64)<0.0001
IABP2.92 (1.42–5.97)0.003
Killip class III or IV6.46 (3.44–12.17)<0.0001
Contrast media (per 10 mL increase)1.03 (1.00–1.06)0.02

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