Predictors of acute kidney injury in patients admitted with ST-elevation myocardial infarction – results from the Bremen STEMI-Registry

Abstract

Background: Deterioration of renal function after exposition to contrast media is a common problem in patients with myocardial infarction undergoing percutaneous coronary interventions. The aim of the present study was to assess the incidence of acute kidney injury in patients admitted with ST-elevation-myocardial infarction (STEMI) and its association with infarction severity, comorbidities and treatment modalities, including amount of contrast media applied. Methods: All patients with STEMI from the metropolitan area of Bremen, Germany are treated at the Bremen Heart Centre and since 2006 documented in the Bremen STEMI-Registry. Acute kidney injury was graded from stage 0 to 3 following the Kidney-disease-improving-global outcomes criteria from 2012. Results: Data from 3810 patients admitted with STEMI were included in this study. No acute kidney injury was observed in 3120 (82%) patients while acute kidney injury was detected in 690 (18%) patients: Stage 1: n=497 (13%), 2: n=66 (2%), 3: n=127 (3%). Acute kidney injury was associated with elevated 30-day (0: 3%, 1: 20%, 2: 46%, 3: 58%) and one-year mortality rates (0: 6%, 1: 26%, 2: 49%, 3: 66%). Higher acute kidney injury stages were associated with higher peak creatine kinase (in U/l±SEM): stage 0: 1748±33, 1: 2588±127, 2: 3684±395, 3: 3330±399, p (<0.01), lower mean systolic blood pressure at admission (in mmHG±SD): 0: 133±28, 1: 129±31; 2: 121±31, 3: 115±33 ( p<0.01) and higher Thrombolysis in Myocardial Infarction risk score for STEMI (scale 0–14±SD): 0: 2.71±2, 1: 4.08±2, 2: 4.98±2, 3: 5.05±2, ( p<0.01). However, no such association could be found between acute kidney injury stage and amount of contrast media applied (in ml±SD) 0: 138±57, 1: 139±61; 2: 140±76; 3: 145±80 ( p=0.5). Reduced initial glomerular filtration rate was associated with higher incidences of acute kidney injury while again no relation to amount of contrast media could be observed in subgroups ranked by initial glomerular filtration rate. A multivariate analysis confirmed these results: while left-heart-failure/cardiogenic shock (odds ratio (OR) 4.2, 95% confidence interval (CI) 3.3–5.5) as well as larger infarctions (peak creatine kinase >3000 U/l (OR 2.2, 95% CI 1.7–2.8)) were independently associated with a greater risk for acute kidney injury, amount of contrast media applied during angiography was not (150–250 ml, OR 0.95, 95% CI 0.8–1.2 ( p=0.7), >250 ml, OR 1.3, 95% CI 0.8–2.0 ( p=0.5)). Conclusions: Acute kidney injury, which was associated with elevated short- and long-term mortality rates, could be observed in 18% of patients admitted with STEMI. The present data suggest that severity and haemodynamic impairment due to STEMI rather than contrast-media-induced nephropathy is the key contributor for acute kidney injury in STEMI patients. The deleterious effect of the myocardial infarction itself on renal function can be explained through renal hypoperfusion, neurohormonal activation or other pathomechanisms that might have been underestimated in the past.