Sepsis is a critical condition resulting from the excessive activation of the inflammatory/immune system in response to an infection, with high mortality if treatment is not administered promptly. One of the many possible complications of sepsis is liver dysfunction with consequent cholestasis. The aim of this paper is to review the main mechanisms involved in the development of cholestasis in sepsis. Cholestasis in a septic patient must raise the suspicion that it is the consequence of the septic condition and limit the laborious attempts of finding a hepatic or biliary disease. Prompt antibiotic administration when sepsis is suspected is essential and may improve liver enzymes. Cholestasis is a syndrome with a variety of etiologies, among which sepsis is frequently overlooked, despite a number of studies and case reports in the literature demonstrating not only the association between sepsis and cholestasis but also the role of cholestasis as a prognostic factor for sepsis‐induced death.

As presepsin levels increase with kidney dysfunction (KD), our aim was to establish cutoff points for presepsin adapted to the level of KD in order to avoid bacterial infection overdiagnosis, antibiotic overprescription, and risk of bacterial resistance. This is a unicenter retrospective study, which included all patients admitted on an emergency basis to 2 departments of a teaching hospital during a 2-year interval to whom presepsin level was determined at the emergency department prior to admission. Serum creatinine (sCrt) was employed to estimate the severity of KD using 3 thresholds (1.5, 2, and 4 mg/dL) resulting in 4 degrees of severity: KD_1, KD_2, KD_3, KD_4. There is an ascending exponential relationship between presepsin and sCrt: presepsin = 600.03e 0.212sCrt . Presepsin levels are significantly different between the patients with KD_1, KD_2, KD_3, and KD_4. In the receiver operating characteristic curves exploring the usefulness of presepsin in sepsis diagnosis, the area under the curve was satisfactory for KD_1 (0.78), KD_2 (0.78), and KD_3 (0.82), but unacceptably low for KD_4 (0.59), while the optimal cutoff points were (depending on the computational method) 700/ 982, 588/ 1125, 1065, and 2260 pg/mL for KD_1, KD_2, KD_3, and KD_4 respectively. The threshold for abnormal presepsin should be about 600, 1000, and 1300 pg/mL in patients with KD_1, KD_2, and KD_3, respectively. In patients with KD_4, presepsin has a poor discriminating power for sepsis diagnosis. If, notwithstanding, it is used for this purpose, the cutoff point should be at least at 2200.

Introduction: Chronic kidney disease (CKD) induces changes in the myocardium known to influence morbidity and mortality, most severe in patients with end stage renal disease. Objectives: The working hypothesis was that in patients on chronic hemodialysis the prevalence of left ventricular diastolic dysfunction is correlated with the inflammatory, oxidative, metabolic, nutritional, and atherosclerotic status. Patients and Methods: An observational study was performed on 51 patients (age 59.76 ± 13.24 years) on hemodialysis treatment. Transthoracic cardiac ultrasound was conducted to evaluate LVDD. The burden of cardiac and arterial atherosclerosis was evaluated by cardiac ultrasound (aortic and mitral valve calcifications), vascular ultrasound (carotid and femoral atheroma plaques, common carotid intima-media thickness), and by abdominal radiography (aortic calcification score). Demographic and anthropometric parameters were determined. Blood samples were used to determine laboratory parameters reflecting the inflammatory, oxidative, and metabolic/nutrition status. Results: LVDD is positively correlated with the serum level of C-reactive protein (CRP) (P=0.04), the total antioxidant capacity of the serum (P=0.04), the presence (P=0.022) and number (P=0.04) of femoral plaques, the aortic calcification score (P=0.02), aortic valve stenosis (P=0.037), aortic annulus calcifications (P=0.02) and mitral valve calcifications (P=0.041). After the removal of the main confounder, degenerative aortic stenosis, only the associations with serum total antioxidant capacity (P=0.04) and aortic calcification score (P= 0.02) maintain their statistical significance. Conclusion: LVDD is positively correlated with inflammation and oxidative stress markers and with the severity of aortic calcification.