Elevated plasma levels of the osteocyte-derived hormone fibroblast growth factor 23 (FGF23) have emerged as a powerful biomarker of cardiovascular disease and death in patients with CKD. Whether elevated urinary or plasma FGF23 levels are prospectively associated with AKI and death in critically ill patients is unknown. We therefore conducted a prospective cohort study of 350 critically ill patients admitted to intensive care units at an academic medical center to investigate whether higher urinary FGF23 levels associate with the composite end point of AKI or in-hospital mortality (AKI/death). We measured urinary FGF23 levels within 24 hours of admission to the intensive care unit. In a subcohort (=131) we also measured plasma levels of FGF23, calcium, phosphate, parathyroid hormone, and vitamin D metabolites. Urinary and plasma FGF23 levels, but not other mineral metabolites, significantly associated with AKI/death. In multivariate analyses, patients in the highest compared with the lowest quartile of urinary FGF23 had a 3.9 greater odds (95% confidence interval, 1.6 to 9.5) of AKI/death. Higher urinary FGF23 levels also independently associated with greater hospital, 90-day, and 1-year mortality; longer length of stay; and several other important adverse outcomes. In conclusion, elevated FGF23 levels measured in the urine or plasma may be a promising novel biomarker of AKI, death, and other adverse outcomes in critically ill patients.

Background Postoperative new-onset atrial fibrillation (PNAF) is the most common complication following cardiac surgery. The pathogenesis of PNAF is multifactorial. The concept of the postoperative inflammatory response, as a potential underlying mechanism has been extensively studied. This review aims to provide a comprehensive summary of literature relevant to the association between the inflammatory response following cardiac surgery and PNAF.

Administration of prophylactic glucocorticoids has been suggested as a strategy to reduce postoperative AKI and other adverse events after cardiac surgery requiring cardiopulmonary bypass. In this post hoc analysis of a large placebo-controlled randomized trial of dexamethasone in 4465 adult patients undergoing cardiac surgery, we examined severe AKI, defined as use of RRT, as a primary outcome. Secondary outcomes were doubling of serum creatinine level or AKI-RRT, as well as AKI-RRT or in-hospital mortality (RRT/death). The primary outcome occurred in ten patients (0.4%) in the dexamethasone group and in 23 patients (1.0%) in the placebo group (relative risk, 0.44; 95% confidence interval, 0.19 to 0.96). In stratified analyses, the strongest signal for potential benefit of dexamethasone was in patients with an eGFR,15 ml/min per 1.73 m 2 . In conclusion, compared with placebo, intraoperative dexamethasone appeared to reduce the incidence of severe AKI after cardiac surgery in those with advanced CKD. 26: 294726: -295126: , 201526: . doi: 10.1681 Acute kidney injury is one of the most ominous complications after cardiac surgery with cardiopulmonary bypass (CPB). Approximately 1% of patients undergoing cardiac surgery require RRT for severe postoperative AKI, and experience strikingly high in-hospital mortality rates exceeding 40%. 1-3 Less severe AKI is far more common and identifies patients still at increased risk of shortand long-term mortality, prolonged length of hospital stay, and higher hospital costs. 4,5 The pathogenesis of AKI after cardiac surgery is complex and includes patient-related factors such as age and comorbidities (e.g., CKD and diabetes mellitus) as well as surgical factors such as type of procedure and duration of CPB. [6][7][8] Cardiac surgery results in a postoperative systemic inflammatory response syndrome due to a variety of factors including surgical trauma, exposure of blood to the artificial surface of the bypass circuit, tissue hypoperfusion, hemolysis, hemodilution, blood transfusion, and hypothermia. 9-12 Inflammation is believed to play a key role in the pathophysiology of AKI after cardiac surgery with CPB. A number of proinflammatory pathways are activated during CPB and can lead to leukocyte extravasation, lipid peroxidation, renal medullary congestion, and tubular cell injury. 1,9 Multiple strategies have been proposed to attenuate the inflammatory response after cardiac surgery with CPB, including the use of glucocorticoids. To date, the effect of glucocorticoids on AKI after cardiac surgery has been evaluated as a primary outcome in 14 randomized controlled trials, the largest of which included 216 patients. 3 A meta-analysis of these studies (which included a total of 888 patients) concluded that glucocorticoids have no protective effect on AKI after cardiac surgery. 3 However, these studies were underpowered, particularly to detect severe AKI. J Am Soc NephrolWe therefore conducted a post hoc analysis of severe AKI in the Dexamethasone for Cardiac Surgery (DE...

No abstract

Liver cirrhosis is a known risk factor for postoperative mortality in patients undergoing cardiac surgery. Clinical assessment of liver cirrhosis using the widely accepted Child-Pugh (CP) score is thus vital for evaluation of surgical options and perioperative care. However, detailed mortality rates as a consequence of liver cirrhosis are unclear. This review aimed to stratify the risk of short-term (<30 days) and overall (up to 10 years) mortality after cardiac surgery in patients with liver cirrhosis, classified by the CP score. Thus, PubMed, Embase, CINAHL and the Cochrane Library were systematically reviewed by two independent investigators for studies published up to February 2014, in which mortality in cirrhotic patients, classified by the CP classification, undergoing cardiac surgery was evaluated postoperatively. A total of 993 articles were identified. After critical appraisal of 21 articles, 19 were selected for final analysis. Weighted short-term mortality of cirrhotic patients undergoing cardiac surgery was 19.3% [95% confidence interval (CI): 16.4-22.5%]. Across the different CP groups, short-term mortality appeared to be 9.0% (95% CI: 6.6-12.2%), 37.7% (95% CI: 30.8-44.3%) and 52.0% (95% CI: 33.5-70.0%) in Groups A, B and C, respectively. Weighted overall mortality within 1 year was 42.0% (95% CI: 36.0-48.3%) in all cirrhotic patients. Subdivided in groups, overall mortality within that 1 year was 27.2% (95% CI: 20.9-34.7%), 66.2% (95% CI: 54.3-76.3%) and 78.9% (95% CI: 56.1-92.1%) in Groups A, B and C, respectively. In conclusion, short-term mortality is considerably increased in patients with liver cirrhosis CP class B and C. Overall mortality is significantly high in all classes of liver cirrhosis.

Despite longer hospital stays and more short-term reoperations for tamponade, patients with PPS had an excellent 1-year prognosis.

Background Postpericardiotomy syndrome (PPS) is a common complication following cardiac surgery; however, the exact pathogenesis remains uncertain. Identifying risk factors of PPS might help to better understand the syndrome. The aim of this study was to provide an overview of existing literature around determinants of PPS in adult cardiac surgery patients.

Arrhythmogenic cardiomyopathy (AC) is characterised by myocardial fibrofatty tissue infiltration and presents with palpitations, ventricular arrhythmias, syncope and sudden cardiac death. AC is associated with mutations in genes encoding the desmosomal proteins plakophilin-2 (PKP2), desmoplakin (DSP), desmoglein-2 (DSG2), desmocollin-2 (DSC2) and junctional plakoglobin (JUP). In the present study we compared 28 studies (2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011) on the prevalence of mutations in desmosomal protein encoding genes in relation to geographic distribution of the study population. In most populations, mutations in PKP2 showed the highest prevalence. Mutation prevalence in DSP, DSG2 and DSC2 varied among the different geographic regions. Mutations in JUP were rarely found, except in Denmark and the Greece/Cyprus region.