AKI is associated with short- and long-term mortality. However, the exact contribution of AKI complications to the burden of mortality and whether RRT has any beneficial effect on reducing mortality rates in critically ill AKI patients are unknown. This was a retrospective analysis using data from the Multiparameter Intelligent Monitoring in Intensive Care II project. A total of 18,410 adult patients were enrolled from four intensive care units from a university hospital from 2001 to 2008. Overall, 10,245 patients developed AKI. After adjustments, the odds ratios (ORs) for hospital mortality were 1.73 (95% confidence interval [95% CI], 1.52 to 1.98) for AKI stage 1, 1.88 (95% CI, 1.57 to 2.25) for stage 2, and 2.89 (95% CI, 2.41 to 3.46) for stage 3. Totals of 33%, 59%, and 70% of the excess mortality rates associated with AKI stages 1, 2, and 3, respectively, were attenuated by the inclusion of each AKI-related complication in the model. The main burden of excess hospital mortality associated with AKI was attenuated by metabolic acidosis and cumulative fluid balance. Long-term mortality was not attenuated by any of the associated complications. Next, we used two different approaches to explore the associations between RRT, AKI complications, and hospital mortality: multivariate analysis and propensity score matching. In both approaches, the sensitivity analysis for RRT was associated with a better hospital survival in only the following AKI-related subgroups: hyperkalemia (OR, 0.55; 95% CI, 0.35 to 0.85), metabolic acidosis (OR, 0.70; 95% CI, 0.53 to 0.92), cumulative fluid balance >5% of body weight (OR, 0.60; 95% CI, 0.40 to 0.88), and azotemia (OR, 0.57; 95% CI, 0.40 to 0.81). A majority of the excess risk of mortality associated with AKI was attenuated by its fluid volume and metabolic complications, particularly in severe AKI. In addition, this study demonstrated that RRT is associated with a better outcome in patients with AKI-related complications.

Background Acute kidney injury (AKI) is an independent risk factor for mortality in adults and children. Generally, urine output (UO) < 1 mL/kg/h is accepted as oliguria in neonates, although it has not been systematically studied. pRIFLE criteria suggest UO cut-offs similar to those of the adult population (0.3 and 0.5 mL/kg/h). The aim of the present study was to investigate UO in correlation with mortality in critically ill neonates and suggest changes in the pRIFLE definition of reduced diuresis. Methods A retrospective cohort study was performed in an eight-bed neonatal intensive care unit (NICU). UO was systematically measured by diaper weight each 3 h. Discriminatory capacity to predict mortality of UO was measured and patients were divided according to UO ranges: G1 > 1.5 mL/kg/h; G2 1.0–1.5 mL/kg/h; G3 0.7–1.0 mL/kg/h and G4 < 0.7 mL/kg/h. These ranges were incorporated to pRIFLE_GFR criteria and its performance was evaluated. Results Of 384 patients admitted at the NICU during the study period, 72 were excluded and overall mortality was 12.8%. UO showed good performance for mortality prediction (area under the curve 0.789, P < 0.001). There was a stepwise increase in hospital mortality according to UO groups after controlling for SNAPPE-II and diuretic use. Using these UO ranges with pRIFLE improves its discriminatory capacity (area under the receiver operating characteristic curve 0.882 versus 0.693, P < 0.05). Conclusions UO is a predictor of mortality in NICU. An association between a UO threshold < 1.5 mL/kg/h and mortality was observed, which is higher than the previously published pRIFLE thresholds. Adopting higher values of UO in pRIFLE criteria can improve its capacity to detect AKI severity in neonates.

In the past 10 years, great effort has been made to define and classify a common syndrome previously known as acute renal failure and now renamed “acute kidney injury (AKI).” Initially suggested and validated in adult populations, AKI classification was adapted to the pediatric population and recently has been modified for the neonatal population. Several studies have been performed in adults and older children using this consensus definition, leading to improvement in the knowledge of AKI incidence and epidemiology. In spite of these advances, the peculiar renal pathophysiology of critically ill newborn patients makes it difficult to interpret urine output (UO) and serum creatinine (SCr) levels in these patients to diagnose AKI. Also, new urine biomarkers have emerged as a possible alternative to diagnose early AKI in the neonatal population. In this review, we describe recent advances in neonatal AKI epidemiology, discuss difficulties in diagnosing AKI in newborns, and show recent advances in new AKI biomarkers and possible long-term consequences after AKI episode.

Leptospirosis is a common disease in tropical countries, and the kidney is one of the main target organs. Membrane proteins of Leptospira are capable of causing endothelial damage in vitro, but there have been no studies in humans evaluating endothelial glycocalyx damage and its correlation with acute kidney injury (AKI). We performed a cohort study in an outbreak of leptospirosis among military personnel. AKI was diagnosed in 14 of 46 (30.4%) patients. Leptospirosis was associated with higher levels of intercellular adhesion molecule-1 (ICAM-1; 483.1 ± 31.7 versus 234.9 ± 24.4 mg/L, P < 0.001) and syndecan-1 (73.7 ± 15.9 versus 21.2 ± 7.9 ng/mL, P < 0.001) compared with exposed controls. Patients with leptospirosis-associated AKI had increased level of syndecan-1 (112.1 ± 45.4 versus 41.5 ± 11.7 ng/mL, P = 0.021) and ICAM-1 (576.9 ± 70.4 versus 434.9 ± 35.3, P = 0.034) compared with leptospirosis patients with no AKI. Association was verified between syndecan-1 and ICAM-1 with serum creatinine elevation and neutrophil gelatinase-associated lipocalin (NGAL) levels. This association remained even after multivariate analysis including other AKI-associated characteristics. Endothelial injury biomarkers are associated with leptospirosis-associated renal damage.

Background: Acute kidney injury (AKI) is a frequent complication in hospitalized patients, especially in those in intensive care units (ICU). The RIFLE classification might be a valid prognostic factor for critically ill cancer patients. The present study aims to evaluate the discriminatory capacity of RIFLE versus other general prognostic scores in predicting hospital mortality in critically ill cancer patients. Methods: This is a single-center study conducted in a cancer-specialized ICU in Brazil. All of the 288 patients hospitalized from May 2006 to June 2008 were included. RIFLE classification, APACHE II, SOFA, and SAPS II scores were calculated and the area under receiver operating characteristic (AROC) curves and logistic multiple regression were performed using hospital mortality as the outcome. Results: AKI, defined by RIFLE criteria, was observed in 156 (54.2%) patients. The distribution of patients with any degree of AKI was: risk, n = 96 (33.3%); injury, n = 30 (10.4%), and failure, n = 30 (10.4%). Mortality was 13.6% for non-AKI patients, 49% for RIFLE ‘R’ patients, 62.3% for RIFLE ‘I’ patients, and 86.8% for RIFLE ‘F’ patients (p = 0.0006). Logistic regression analysis showed that RIFLE criteria, APACHE II, SOFA, and SAPS II were independent factors for mortality in this population. The discrimination of RIFLE was good (AROC 0.801, 95% CI 0.748–0.854) but inferior compared to those of APACHE II (AROC 0.940, 95% CI 0.915–0.966), SOFA (AROC 0.910, 95% CI 0.876–0.943), and SAPS II (AROC 0.869, 95% CI 0.827–0.912). Conclusion: AKI is a frequent complication in ICU patients with cancer. RIFLE was inferior to commonly used prognostic scores for predicting mortality in this cohort of patients.