Prognostic value of midregional proadrenomedullin in critically ill patients.

INTRODUCTION: Scoring systems can be used to predict the risk of mortality and outcomes in critically ill patients. Acute kidney injury (AKI) is one of the strongest factors negatively influencing patient outcomes. Midregional proadrenomedullin (MR­proADM) shows promising results as an outcome predictor in patients with sepsis. OBJECTIVES: We aimed to evaluate the value of MR­proADM in incident AKI and mortality prognostication among patients admitted to the intensive care unit (ICU) in comparison with commonly used scoring systems. PATIENTS AND METHODS: Our study included a single­center cohort of 77 patients admitted to the ICU. Plasma MR­proADM levels were measured within 24 h of admission. The Acute Physiology and Chronic Health Evaluation II (APACHE II) and the Sequential Organ Failure Assessment (SOFA) scores were used as a reference. The primary endpoints were incident AKI and in­hospital mortality. RESULTS: Patients who died during hospitalization period had a higher MR­proADM concentrations as compared with patients who survived (2592.5 pg/ml vs 995.3 pg/ml; P <0.001). The levels of MR­proADM correlated positively with the APACHE II or SOFA score (r = 0.3; P = 0.004 and r = 0.3; P = 0.008, respectively). In the receiver operating characteristics analysis, MR­proADM concentration was superior to both scoring systems (P = 0.002 and P = 0.001, respectively). In univariate logistic regression, MR­proADM was associated with in­hospital mortality (odds ratio [OR], 1.22; 95% CI, 1.11-1.35 per 100 pg/ml increase of MR­proADM) and after adjusting for multiple variables remained an independent predictor of death (OR, 1.35; 95% CI, 1.22-1.49 per 100 pg/ml increase of MR­proADM). MR­proADM was not useful in predicting incident AKI. CONCLUSIONS: MR­proADM can be applied in clinical practice as a prognostic tool for mortality but not incident AKI in the general ICU population with at least similar accuracy as APACHE II and SOFA scores.

C-terminal and intact FGF23 in critical illness and their associations with acute kidney injury and in-hospital mortality.

BACKGROUND: FGF23 proved its value in prognostication of cardiovascular events and mortality among renal patients and general population. Limited data exist whether FGF23 may have any use in prediction of negative outcomes among critically ill patients admitted to intensive care unit (ICU). METHODS: Single center cohort study performed among patients admitted to ICU. The primary exposure was FGF23 plasma concentration measured within 24 h of ICU admission. The primary outcome was incident Acute Kidney Injury (AKI) and in-hospital mortality during the ICU stay. RESULTS: The study enrolled 79 patients admitted to ICU. C-terminal FGF23 (cFGF23) but not intact FGF23 (iFGF23) concentration was significantly elevated in patients, who acquired AKI and non-survivors (p < .001). ROC analysis of cFGF23 yielded an AUC of 0.81 and 0.85 for prediction of incident AKI and death during ICU stay, respectively. Multivariate analysis showed higher odds for AKI (OR 1.80; 95% CI 1.10-2.96) and in-hospital mortality (OR 2.85; 95% CI 1.60-5.06) for one unit increase of log transformed cFGF23. CONCLUSIONS: cFGF23 measurement may serve as a novel biomarker for incident AKI and death among critically ill patients.

[Post-resuscitation syndrome--management]. / Zespól poresuscytacyjny--postepowanie terapeutyczne.

Despite cardiopulmonary resuscitation guidelines and their regular updates, the results of cardiac arrest victims treatment are still disappointingly poor. Complex treatment including providing artificial ventilation, circulatory support and prevention of secondary damage from ischemia and hypoxia is a complicated process and its result is unpredictable. The aim of the paper is to present the main steps in post-resuscitation syndrome treatment including ventilatory and circulatory stabilization, central nervous system protection and prognostic value of biochemical and neurophysiological tests.

Molecular basics of sepsis developement.

Bacterial infections and sepsis remain major causes of morbidity and mortality in intensive care units. The normal host response to infection is a complex process that serves to localise and control the invasion of microbes and to repair injured tissue. Local inflammatory processes are regulated through the production of cytokines by macrophages. In some cases, mediator release exceeds the boundaries of the local environment and results in the development of sepsis. It is well known that the innate immune system plays a crucial role in preventing microbial invasion. The human innate immune system consists of genetically programmed defence mechanisms that are directed against molecular components found only in microorganisms. Understanding the complexity of early response to infection with respect to innate immune response is required for the future development of drugs that will effectively control infectious diseases.