Development of acute kidney injury (AKI) following primary percutaneous coronary intervention (PCI) is not related to the use of contrast media, but rather to factors such as older age and hemodynamic instability, according to a new study.
The study included 2025 patients with ST-segment-elevation myocardial infarction (STEMI) who underwent primary PCI and received non-ionic, low-osmolar, iodinated contrast agents and a control group of 1025 STEMI patients who received fibrinolysis or no reperfusion and were not exposed to contrast media during the first 72 hours of their hospital stay.
The researchers defined AKI as an increase in serum creatinine concentration of 0.5 mg/dL or higher compared with admission values or a greater than 25% relative rise during the first 72 hours after the PCI.
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Results demonstrated no statistically significant difference in AKI rates between the PCI and control groups (10.3% vs. 12.1%), Oren Caspi, MD, PhD, of the Rambam Medical Center in Haifa, Israel, and colleagues reported online in the Journal of the American Heart Association.
AKI rates also showed no statistically significant difference in AKI rates when investigators compared 931 PCI patients with 931 propensity score-matched controls (8.6% vs 10.9%).
AKI developed in 209 (10.3%) of the 2025 PCI patients. The median contrast dose was 160 mL in the AKI patients and 150 mL in the patients without AKI, a difference that was not statistically significant.
“It is unlikely that contrast media exposure is a primary pathogenic factor responsible for renal dysfunction following primary PCI,” the authors wrote.
In multivariate analysis, statistically significant independent predictors of AKI in the PCI group included age 70 years or older, baseline estimated glomerular filtration rate (eGFR), insulin-treated diabetes, heart failure and hemodynamic instability, and decreased left ventricular ejection fraction (LVEF), but not contrast volume. Patients aged 70 years and older had 1.9 times greater odds of AKI than younger patients. Patients with an eGFR less than 30 and 30–59 mL/min/1.73 m2 had 1.7- and 6.3-fold greater odds of AKI compared with those who had an eGFR of 60 mL/min/1.73 m2 or higher. Compared with non-diabetics, those with insulin-treated diabetes had 2-fold greater odds of AKI. Patients in Killip class II-III had 2.2-fold greater odds of AKI compared with those in Killip class I. Patient in Killip class IV or who used an intra-aortic balloon pump had 6.6-fold higher odds of AKI. An LVEF below 45% was associated with 1.7-fold higher odds of AKI.
Attempts to reduce AKI rates in STEMI patients likely require targeting mechanisms unrelated to contrast media, the authors stated.
Reference
Caspi O, Habib M, Cohen Y, et al. Acute kidney injury after primary angioplasty: Is contrast-induced nephropathy the culprit? J Am Heart Assoc 2017;6:e005715. doi: 10.1161/JAHA.117.005715
