Association Between Minimum Inhibitory Concentration, Beta-lactamase Genes and Mortality for Patients Treated With Piperacillin/Tazobactam or Meropenem From the MERINO Study.

INTRODUCTION: This study aims to assess the association of piperacillin/tazobactam and meropenem minimum inhibitory concentration (MIC) and beta-lactam resistance genes with mortality in the MERINO trial. METHODS: Blood culture isolates from enrolled patients were tested by broth microdilution and whole genome sequencing at a central laboratory. Multivariate logistic regression was performed to account for confounders. Absolute risk increase for 30-day mortality between treatment groups was calculated for the primary analysis (PA) and the microbiologic assessable (MA) populations. RESULTS: In total, 320 isolates from 379 enrolled patients were available with susceptibility to piperacillin/tazobactam 94% and meropenem 100%. The piperacillin/tazobactam nonsusceptible breakpoint (MIC >16 mg/L) best predicted 30-day mortality after accounting for confounders (odds ratio 14.9, 95% confidence interval [CI] 2.8-87.2). The absolute risk increase for 30-day mortality for patients treated with piperacillin/tazobactam compared with meropenem was 9% (95% CI 3%-15%) and 8% (95% CI 2%-15%) for the original PA population and the post hoc MA populations, which reduced to 5% (95% CI -1% to 10%) after excluding strains with piperacillin/tazobactam MIC values >16 mg/L. Isolates coharboring extended spectrum ß-lactamase (ESBL) and OXA-1 genes were associated with elevated piperacillin/tazobactam MICs and the highest risk increase in 30-day mortality of 14% (95% CI 2%-28%). CONCLUSIONS: After excluding nonsusceptible strains, the 30-day mortality difference from the MERINO trial was less pronounced for piperacillin/tazobactam. Poor reliability in susceptibility testing performance for piperacillin/tazobactam and the high prevalence of OXA coharboring ESBLs suggests that meropenem remains the preferred choice for definitive treatment of ceftriaxone nonsusceptible Escherichia coli and Klebsiella.

Type I cardiorenal syndrome in patients with acutely decompensated heart failure: the importance of new renal biomarkers.

OBJECTIVE: Type 1 cardiorenal syndrome (CRS) is an acute renal failure in patients with acute decompensated heart failure with an incidence of 24% to 45%. The aim of our study was to investigate the significance of new renal biomarkers to predict type 1 CRS. PATIENTS AND METHODS: The study included 111 patients with acute decompensated heart failure diagnosed at the Istanbul Medical Faculty Emergency Department between 2014 and 2016, and 24 healthy volunteers. All urine samples were stored at -80°C after centrifugation. Samples were run according to the instructions of TIMP-2, ILGF-7, KIM-1, and IGFBP-7 ELISA kits. Diuretic treatments were then administered with intravenous administration of at least 80 mg furosemide per day. Follow-up biochemical and spot urine specimens were taken after 72 hours. For statistical analysis, SPSS version 21.0 statistical software was used. Significance was evaluated at p<0.05. RESULTS: The baseline creatinine level was measured as 1.33 ± 0.39 mg/dL in the heart failure group. It was seen that 67% (75) of the patients had increased creatinine levels and developed type 1 CRS. ILGF-7, TIMP-2, and (ILGF-7 * TIMP-2) values were significantly higher in patients with cardiorenal syndrome when we separated the two groups as patients with and without cardiorenal syndrome (0.40 (0.25-0.71), p1: 0.049/2.40 (1.42-3.70), p2: 0.003/1.15 (0.29-2.43), p3: 0.001). CONCLUSIONS: Renal tubular markers reveal promising developments in the pathophysiology of cardiorenal syndrome in light of recently obtained data. Renal tubular biomarkers may have the potential to be a predictor of heart failure and cardiorenal syndrome.

Coseismic and Postseismic Fault Slip for the 17 August 1999, M = 7.5, Izmit, Turkey Earthquake.

We use Global Positioning System (GPS) observations and elastic half-space models to estimate the distribution of coseismic and postseismic slip along the Izmit earthquake rupture. Our results indicate that large coseismic slip (reaching 5.7 meters) is confined to the upper 10 kilometers of the crust, correlates with structurally distinct fault segments, and is relatively low near the hypocenter. Continued surface deformation during the first 75 days after the earthquake indicates an aseismic fault slip of as much as 0.43 meters on and below the coseismic rupture. These observations are consistent with a transition from unstable (episodic large earthquakes) to stable (fault creep) sliding at the base of the seismogenic zone.