Acute kidney injury in the setting of acute ST-elevation myocardial infarction

Purpose: Acute Kidney Injury (AKI) is mostly defined as an increase in serum creatinine and is observed in up to 19% of ST-Elevation Myocardial Infarction (STEMI) patients. Important mechanisms of AKI in STEMI patients are renal hypoperfusion due to a large infarcts, the use of nephrotoxic agents in particular during Primary Percutaneous Coronary Intervention (PPCI), activation of sympathetic and renin-angiotensin-aldosteron system, inflammation, etc. Our purpose was to evaluate the incidence of AKI in STEMI patients, the impact of AKI upon survival in STEMI patients and predictors of AKI in STEMI patients. Methods: We retrospectively evaluated 681 STEMI patients, admitted in 2008-2010 (68,9% men, mean age 63.6±12.6 years). Reperfusion strategy was PPCI combined with antithrombotic therapy. AKI was defined as an increase of serum creatinine of more than 50% within 24-48 hours. We registered 30-day and six-month mortality in all STEMI patients, survival in AKI-STEMI subpopulation and predictors of AKI such as reperfusion strategy (PPCI), markers of ischemic necrosis (admission and peak troponin I), of inflammation (admission CRP) and of in-hospital heart failure (in-hospital EF and NT-proBNP). Results: PPCI was performed in 89.7% of all STEMI patients. AKI was observed in 12.3%. 30-day mortality of all STEMI patients was 12.5%, six-month mortality 15.4%. In STEMI patients with AKI survival was less likely than in non-AKI patients within 30 days (41.7% vs 94%, p<0.001) and within six months (34.6% vs 91.7%, p<0.001). AKI-STEMI patients in comparison to non-AKI ones were significantly older (69.6±11 vs 62.7±12.5 years, p<0.001) with significantly increased mean admission troponin I (20.7±30.5 μg/l vs 10.6±22.3 μg/l, p<0.001) and peak troponin I (64.6±37.7 μg/l vs 47.2±35.2 μg/l, p<0.001), admission CRP (26.9±54 mg/l vs 14.3±32.3 mg/l, p<0.003) and in-hospital NT-proBNP (1642±1275 vs 528.4±843.7 pmol/l, p<0.001), but significatly decreased in-hospital EF (32.3±15.9% vs 45.4±13.0%, p<0.001), less likely performed PPCI (76.1% vs 91.6%, p<0.001) in particularly within 12 hours of chest pain (63% vs 77.5%, p<0.04). Most significant independent predictor of AKI in STEMI patients was in-hospital NT-proBNP (c2 13.433, OR 1.002, 95% CI 1.001 to 1.003, p<0.001) as demonstrated by logistic regression. Conclusions: AKI was present in more than 10% of STEMI patients and associated with less frequent and later performance of PPCI, increased NT-proBNP and decreased survival. Increased NT-proBNP, being a marker of heart failure seemed most significant predictor of AKI in STEMI patients.