Impact of acute kidney injury on clinical outcomes after ST elevation acute myocardial infarction.

PURPOSE: This study aimed to compare the incidence and clinical significance of transient versus persistent acute kidney injury (AKI) on acute ST elevation myocardial infarction (STEMI). MATERIALS AND METHODS: The study was a retrospective cohort of 855 patients with STEMI. AKI was defined as an increase of ≥0.3 mg/dL in creatinine level at any point during hospital stay. The study population was classified into 5 groups: 1) patients without AKI; 2) patients with mild AKI that was resolved by discharge (creatinine change less than 0.5mg/dL compared with admission creatinine during hospital stay, transient mild AKI); 3) patients with mild AKI that did not resolve by discharge (persistent mild AKI); 4) patients with moderate/severe AKI that was resolved by discharge (creatinine change more than 0.5 mg/dL compared with admission creatinine, transient moderate/severe AKI); 5) patients with moderate/ severe AKI that did not resolve by discharge (persistent moderate/severe AKI). We investigated 1-year all-cause mortality after hospital discharge for the primary outcome of the study. The relation between AKI and 1-year mortality after STEMI was analyzed. RESULTS: AKI occurred in 74 (8.7%) patients during hospital stay. Adjusted hazard ratio for mortality was 3.139 (95% CI 0.764 to 12.897, p=0.113) in patients with transient, mild AKI, and 8.885 (95% CI 2.710 to 29.128, p<0.001) in patients with transient, moderate/severe AKI compared to patients without AKI. Persistent moderate/severe AKI was also independent predictor of 1 year mortality (hazard ratio, 5.885; 95% CI 1.079 to 32.101, p=0.041). CONCLUSION: Transient and persistent moderate/severe AKI during acute myocardial infarction is strongly related to 1-year all cause mortality after STEMI.

Inverse association of peripheral blood CD4(+) invariant natural killer T cells with atopy in human asthma.

Invariant natural killer T (iNKT) cells have been reported to play a role in the pathogenesis of murine asthma. However, the role for iNKT cells in the pathogenesis of human asthma is not defined. In this study we aimed to determined how blood iNKT cells are associated with atopy in asthmatic individuals. Peripheral blood mononuclear cells were isolated from 45 asthmatic subjects. iNKT cells were stained with 6B11 mAb, anti-TCRvalpha24 mAb, or alpha-galactosylceramide (GalCer)-loaded CD1d- tetramer and analyzed with flow-cytometric assays. Increased serum total IgE or one or more positive skin reactions to common allergens were used as atopic indexes. Asthmatic subjects with IgE > 500 IU/ml showed lower frequency of CD4(+) 6B11(+) iNKT cells (p < 0.01) or CD4(+) Valpha24(+) iNKT cells (p < 0.01) compared with subjects with IgE < or = 500 IU/ml. Asthmatic subjects with atopy on skin tests had lower frequency of CD4(+) alpha-GalCer-loaded CD1d- tetramer(+) iNKT cells compared with those without atopy (p < 0.05). The frequency of CD4(+) Valpha24(+) iNKT cells was negatively correlated with total IgE in asthmatic subjects (r = -0.33, p < 0.05). In summary, blood CD4(+) iNKT cells were inversely associated with atopic indexes in asthmatic individuals. We hypothesize that blood CD4(+) iNKT cells might behave like T(h)1-like iNKT cells in human asthma.