Subclinical and clinical contrast-induced acute kidney injury: data from a novel blood marker for determining the risk of developing contrast-induced nephropathy (ENCINO), a prospective study.

OBJECTIVE: Neutrophil gelatinase-associated lipocalin (NGAL) is produced in response to tubular injury. Contrast-induced acute kidney injury (CI-AKI) is associated with adverse outcomes in chronic kidney disease (CKD) patients. We sought to characterize blood NGAL level and the degree of kidney injury in CKD patients who underwent coronary angiography. METHODS: This study was a prospective, blinded assessment of blood samples obtained from patients with estimated glomerular filtration rates (eGFRs) between 15 and 90 mL/min/1.73 m2 undergoing elective coronary angiography with iodinated contrast. Blood NGAL and serum creatinine were measured at baseline, 1, 2, 4, 6, 12, 24 and 48 h after contrast administration. RESULTS: A total of 63 subjects with a mean eGFR of 48.17±16.45 mL/min/1.73 m2 were enrolled. There was a graded increase in baseline NGAL levels across worsening stages of CKD (p=0.0001). Post-procedure NGAL increased from baseline in each stage of CKD. Eight (12.7%) patients were diagnosed with CI-AKI by diagnostic criteria of 2012 KDIGO definition of CI-AKI, and seven (11.1%) patients developed subclinical CI-AKI defined by a twofold or greater rise in NGAL. There was no relationship between baseline eGFR and diabetes on the composite outcome of subclinical and clinical CI-AKI. CONCLUSIONS: Baseline and post-procedure NGAL are progressively elevated according to the baseline stage of CKD. Using a twofold rise in NGAL, 46.7% of composite CI-AKI is detected and complements the 53.3% of cases identified using KDIGO criteria. Traditional risk predictors were not independently associated with this composite outcome.

Malignant ventricular arrhythmias in patients with acute right ventricular infarction undergoing mechanical reperfusion.

Patients with acute right ventricular (RV) infarctions are prone to ventricular arrhythmias, but little is known regarding the temporal patterns of these arrhythmias, their impact on outcomes, or their relation to the severity of RV impairment. The aim of this study was to examine the impact of malignant ventricular arrhythmias (MVAs) complicating acute RV infarction. A further aim was to determine whether the degree of RV impairment was a predisposing factor to MVAs. The charts of 48 patients with acute RV infarctions were reviewed for documented MVAs. Temporal presentation, relating to reperfusion, and in-hospital outcomes were tabulated. Echocardiograms were reviewed to quantify RV impairment. MVAs occurred in 38% of patients, with multiple episodes (electrical storm) in 8.3%. MVAs developed before reperfusion (72% of patients), abruptly with reperfusion (11%), or after reperfusion (22%). Patients with MVAs had larger infarcts (peak creatine phosphokinase 3,027 vs 1,848 U/L, p = 0.03) and trended toward worse RV function (fractional shortening 27% vs 34%, p = 0.08). In-hospital mortality (patients with MVAs 17% vs 6.7%, p = 0.35), intensive care days (patients with MVAs 7.1 +/- 10 vs 3.9 +/- 2.5, p = 0.39), and hospital days (patients with MVAs 10.3 +/- 10 vs 8.0 +/- 5.1, p = 0.57) were similar between groups. Patients with electrical storm had longer intensive care stays (18.0 +/- 18.5 vs 4.0 +/- 2.5 days, p = 0.02) and hospital stays (20.5 +/- 17 vs 7.9 +/- 5.0 days, p = 0.05). In conclusion, MVAs are common in acute RV infarctions. They frequently occur before reperfusion and are associated with larger infarcts. With reperfusion, MVAs had little impact on intensive care and hospital stays or in-hospital mortality, except in patients with electrical storm.