Acute kidney injury (AKI) is a frequent complication after cardiac surgery and is associated with increased mortality. The aim was to design a nondialytic AKI score in patients with previously normal renal function undergoing cardiac surgery. Data were collected on 909 patients who underwent cardiac surgery with cardiopulmonary bypass between 2012 and 2014. A total of 810 patients fulfilled the inclusion criteria. Patients were classified as having AKI based on the RIFLE criteria. Postoperative AKI occurred in 137 patients (16.9%). Several parameters were recorded preoperatively, intraoperatively, and at intensive care unit admission, looking for a univariate and multivariate association with AKI risk. A second data set of 741 patients, from 2 different hospitals, was recorded as a validation cohort. Four independent risk factors were included in the CRATE score: creatinine (odds ratio [OR], 9.66; 95% confidence interval [CI], 4.77-19.56; P < .001), EuroSCORE (OR, 1.40; CI, 1.29-1.52; P < .001), lactate (OR, 1.03; CI, 1.01-1.04; P < .001), and cardiopulmonary bypass time (OR, 1.01; CI, 1.01-1.02; P < .001). The accuracy of the model was good, with an area under the curve of 0.89 (CI, 0.85-0.92). The CRATE score retained good discrimination in validation cohort, with an area under the curve of 0.81 (95% CI, 0.78-0.85). CRATE score is an accurate and easy to calculate risk score that uses affordable and widely available variables in the routine care surgical patients.

Goal-directed therapy based on brain-oxygen saturation (bSo₂) is controversial and hotly debated. While meta-analyses of aggregated data have shown no clinical benefit for brain near-infrared spectroscopy (NIRS)-based interventions after cardiac surgery, no network meta-analyses involving both major cardiac and noncardiac procedures have yet been undertaken. Randomized controlled trials involving NIRS monitoring in both major cardiac and noncardiac surgery were included. Aggregate-level data summary estimates of critical outcomes (postoperative cognitive decline (POCD)/postoperative delirium (POD), acute kidney injury, cardiovascular events, bleeding/need for transfusion, and postoperative mortality) were obtained. NIRS was only associated with protection against POCD/POD in cardiac surgery patients (pooled odds ratio (OR)/95% confidence interval (CI)/I²/number of studies (n): 0.34/0.14–0.85/75%/7), although a favorable effect was observed in the analysis, including both cardiac and noncardiac procedures. However, the benefit of the use of NIRS monitoring was undetectable in Bayesian network meta-analysis, although maintaining bSo₂ > 80% of the baseline appeared to have the most pronounced impact. Evidence was imprecise regarding acute kidney injury, cardiovascular events, bleeding/need for transfusion, and postoperative mortality. There is evidence that brain NIRS-based algorithms are effective in preventing POCD/POD in cardiac surgery, but not in major noncardiac surgery. However, the specific target bSo₂ threshold has yet to be determined.

Major changes have occurred in the epidemiology and etiology of infective endocarditis (IE). Nevertheless, the differences between nosocomial infective endocarditis (NIE) and community-acquired infective endocarditis (CIE) have not been addressed in a population-based study. We conducted a retrospective, nationwide, temporal trend study from 1997 to 2014 analyzing the epidemiology, clinical, geographical, meteorological characteristics of patients diagnosed with IE in Spain, to distinguish NIE from CIE. Among 25,952 patients with IE (62.2 ± 18·6 years; 65.9% men), 45.9% had NIE. The incidence of IE increased from 2.83 to 3.73 due to the NIE incidence increment with a decline in CIE. Patients with NIE were older (63.8 years vs. 60.8 years, p < 0·001), presented a higher Charlson index (1.22 vs. 1.03, p < 0.001), a greater history of implanted cardiac devices (8.7% vs. 4.6%, p < 0.001), and higher mortality (31.5% vs. 21.7%, p < 0.001). The most frequent microorganism for both NIE and CIE was Staphylococcus (p < 0.001), and the North reported a higher incidence (p < 0.001). Risk factors of mortality for NIE were age, Charlson index, hemodialysis, shock, heart failure, and stroke. Risk factors for CIE included female sex, renal disease, and cardiac-device carriers. The etiology of IE shifted from community origins to mostly nosocomial-associated infections. Higher morbidity, mortality, and poorer outcomes are associated with NIE.

The aims of this study were to identify the risk factors associated with acute kidney injury (AKI) after isolated surgical revascularization with cardiopulmonary bypass and to develop a model to predict the appearance of postoperative AKI. A total of 435 adult patients who underwent primary isolated coronary artery bypass graft (CABG) surgery, from 2012 to 2016, in the Clinic University Hospital of Valladolid (Spain) were enrolled. AKI was defined according to the risk, injury, failure, loss, and end-stage (RIFLE) criteria. Data were collected from hospital electronic medical records. Multiple logistic regression analysis was used to identify risk factors. The prevalence of AKI was 12.4%. Multivariate analysis identified age (odds ratio [OR], 1.056; 95% confidence interval [CI], 1.016-1.098; P=0.005), hypertension (OR, 3.078; 95% CI, 1.151-8.230; P=0.018), low ejection fraction (EF) (OR, 6.785; 95% CI, 2.080-22.135; P=0.001), estimated glomerular filtration rate (eGFR) (OR, 1.017; 95% CI, 1.005-1.028; P=0.014), EuroSCORE II (OR, 1.049; 95% CI, 1.004-1.096; P=0.033), and no intake of calcium-channel blockers (CCB) (OR, 4.892; 95% CI, 1.496-16.025; P=0.022) as risk factors for AKI. These risk factors were included in a model to predict postoperative AKI with an area under a receiver operating characteristic curve of 0.783±0.036 (95% CI, 0.713-0.854; P<0.0001). Age, hypertension, low EF, eGFR, EuroSCORE II, and no intake of CCB were independent risk factors for postoperative AKI. These factors provide an easy and accurate model to predict postoperative AKI in patients undergoing cardiac surgery.

Acute kidney injury (AKI) is a widely held concern related to a substantial burden of morbidity, mortality and expenditure in the healthcare system. AKI is not a simple illness but a complex conglomeration of syndromes that often occurs as part of other syndromes in its wide clinical spectrum of the disease. Genetic factors have been suggested as potentially responsible for its susceptibility and severity. As there is no current cure nor an effective treatment other than generally accepted supportive measures and renal replacement therapy, updated knowledge of the genetic implications may serve as a strategic tactic to counteract its dire consequences. Further understanding of the genetics that predispose AKI may shed light on novel approaches for the prevention and treatment of this condition. This review attempts to address the role of key genes in the appearance and development of AKI, providing not only a comprehensive update of the intertwined process involved but also identifying specific markers that could serve as precise targets for further AKI therapies.