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Background The presence of chronic kidney disease is an independent prognostic factor in patients with myocardial infarction (MI). We compared the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation and the Modification of Diet in Renal Disease (MDRD) study equation with regard to prognostic value in patients with MI. Methods This study analyzed a retrospective cohort of 11 050 consecutive patients who had MI and were enrolled in the Korea Acute Myocardial Infarction Registry from November 2005 to August 2008. We applied the CKD-EPI equation and the MDRD study equation to determine the estimated glomerular filtration rate (eGFR) in a cohort of patients with MI. Results The mean eGFRCKD-EPI was slightly higher than that of eGFRMDRD (73.16 versus 72.23 mL/min/1.73 m2; P < 0.001). The prevalence of eGFRCKD-EPI <60 mL/min/1.73 m2 was 26.9%, whereas that of eGFRMDRD was 28.5%. The area under the receiver operating characteristic curve was significantly larger for predicting the 1-year major adverse cardiovascular event (MACE) and 1-year all-cause mortality with CKD-EPI equation (0.648 versus 0.641, 0.768 versus 0.753, respectively; P < 0.001). The net reclassification index for improvement in risk of 1-year MACE and 1-year all-cause mortality were 4.09% (P< 0.001) and 9.25% (P< 0.001), respectively. Conclusions The application of the eGFRCKD-EPI demonstrated better predictive values for clinical outcomes than eGFRMDRD in a cohort of patients with MI. [ABSTRACT FROM PUBLISHER]

Background. The aldehyde products of lipid peroxidation such as 4-hydroxy-2-hexenal (HHE) might be responsible for the pathogenesis of kidney injury. The present study was aimed to investigate the effects of HHE on renal tubular epithelial cells and its signaling mechanisms.Methods. Human proximal tubular epithelial (HK-2) cells were treated with 10 μM of HHE. Cell viability was examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The fluorescent probe 2′,7′-dichlorofluorescein diacetate was used to measure intracellular levels of reactive oxygen species (ROS). The protein expression of NF-κB, mitogen-activated protein kinase (MAPK), pro-apoptoic Bax and anti-apoptotic protein Bcl-2 was determined by semiquantitative immunoblotting. Apoptosis was assessed by flow cytometry analysis after the cells were stained by fluorescein isothiocyanate-conjugated annexin V protein and propidium iodine.Results. Treatment with various doses of HHE resulted in dose-dependent decreases of cell viability and increases of ROS. HHE increased the expression of p38 MAPK, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). HHE induced NF-κB activation and IκB-α degradation. Increased nuclear NF-κB activation was blocked by inhibitors of ERK (PD98059) or JNK (SP600125), but not affected by p38 MAPK inhibitor (SB203580). Flow cytometry analysis revealed HHE-induced apoptosis. HHE decreased the expression of Bcl-2, while it increased that of Bax, which was attenuated by the treatment of NF-κB inhibitor (Bay 11-7082) or N-acetyl-L-cysteine (NAC). An inhibition of NF-κB prevented HHE-induced apoptosis.Conclusions. HHE-induced tubular cell apoptosis is mediated by modulation of Bax and Bcl-2 via ROS generation. HHE-mediated accumulation of ROS may induce redox-sensitive transcription factor, NF-κB, through activation of ERK and JNK, resulting in cellular apoptosis in HK-2 cells. [ABSTRACT FROM PUBLISHER]