Background. Currently, evidence regarding the predictive significance of red blood cell distribution width (RDW) among patients with acute respiratory distress syndrome (ARDS) remains scarce. The aim of this study was to determine the prognostic value of RDW for critically ill patients with ARDS. Methods. We studied all patients with ARDS from the Multiparameter Intelligent Monitoring in Intensive Care Database III (MIMIC-III) for whom RDW was available. The clinical outcomes were 30-day and 90-day mortality. Analyses included logistic multivariate regression model, Receiver Operating Characteristic (ROC) analysis, and subgroup analysis. Results. A total of 404 eligible ARDS patients were included. After adjustment for several clinical characteristics related to 30-day mortality, the adjusted OR (95% CIs) for RDW levels ≥14.5% was 1.91 (1.08, 3.39). A similar trend was observed for 90-day mortality. The RDW levels ≥14.5% were also an independent predictor of 90-day mortality (OR, 2.56; 95% CI, 1.50 to 4.37; P = 0.0006) compared with the low RDW levels (<14.5%). In subgroup analyses, RDW showed no significant interactions with other relevant risk factors for 30-day mortality. Conclusions. RDW appeared to be a novel, independent predictor of mortality in critically ill patients with ARDS.

There has been no study exploring the prognostic values of neutrophil percentage-to-albumin ratio (NPAR). We hypothesised that NPAR is a novel marker of inflammation and is associated with all-cause mortality in patients with severe sepsis or septic shock. Patient data were extracted from the MIMIC-III V1.4 database. Only the data for the first intensive care unit (ICU) admission of each patient were used and baseline data were extracted within 24 h after ICU admission. The clinical endpoints were 30-, 90- and 365-day all-cause mortality in critically ill patients with severe sepsis or septic shock. Cox proportional hazards models and subgroup analyses were used to determine the relationship between NPAR and these clinical endpoints. A total of 2166 patients were eligible for this analysis. In multivariate analysis, after adjustments for age, ethnicity and gender, higher NPAR was associated with increased risk of 30-, 90- and 365-day all-cause mortality in critically ill patients with severe sepsis or septic shock. Furthermore, after adjusting for more confounding factors, higher NPAR remained a significant predictor of all-cause mortality (tertile 3 vs. tertile 1: HR, 95% CI: 1.29, 1.04–1.61; 1.41, 1.16–1.72; 1.44, 1.21–1.71). A similar trend was observed in NPAR levels stratified by quartiles. Higher NPAR was associated with increased risk of all-cause mortality in critically ill patients with severe sepsis or septic shock.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and devastating clinical disorders with high mortality and no specific therapy. An excessive inflammatory response results in the progression of ALI/ARDS, and the NLRP3 inflammasome is a key participant in inflammation. Erythropoietin (EPO), which is clinically used for anemia, reportedly exerts pleiotropic effects in ALI. However, whether EPO could protect against lipopolysaccharide (LPS)-induced ALI by regulating the NLRP3 inflammasome and its underlying mechanisms remain poorly elucidated. This study aimed to explore whether the therapeutic effects of EPO rely on the suppression of the NLRP3 inflammasome and the specific mechanisms in an LPS-induced ALI mouse model. ALI was induced in C57BL/6 mice by intraperitoneal (i.p.) injection of LPS (15 mg/kg). EPO was administered intraperitoneally at 5 U/g after LPS challenge. The mice were sacrificed 8 h later. Our findings indicated that application of EPO markedly diminished LPS-induced lung injury by restoring histopathological changes, lessened lung wet/dry (W/D) ratio, protein concentrations in bronchoalveolar lavage fluid (BALF) and myeloperoxidase (MPO) levels. Meanwhile, EPO evidently decreased interleukin-1β (IL-1β) and interleukin-18 (IL-18) secretion, the expression of NLRP3 inflammasome components including pro-IL-1β, NLRP3, and cleaved caspase-1 as well as phosphorylation of nuclear factor-κB (NF-κB) p65, which may be associated with activation of EPO receptor (EPOR), phosphorylation of Janus-tyrosine kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3). However, all the beneficial effects of EPO on ALI and modulation NLRP3 inflammasome were remarkably abrogated by the inhibition of EPOR/JAK2/STAT3 pathway and knockout (KO) of NLRP3 gene. Taken together, this study indicates that EPO can effectively attenuate LPS-induced lung injury in mice by suppressing the NLRP3 inflammasome, which is dependent upon activation of EPOR/JAK2/STAT3 signaling and inhibition of the NF-κB pathway.

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Background. No epidemiological study has investigated the effect of anion gap (AG) on the prognosis of critically ill patients with acute kidney injury (AKI). Therefore, we aimed to determine the association between serum AG and all-cause mortality in these patients. Methods. From MIMIC III, we extracted demographics, vital signs, laboratory tests, comorbidities, and scoring systems from the first 24 h after patient ICU admission. A generalized additive model was used to identify a nonlinear association between anion gap and 30-day all-cause mortality. We also used the Cox proportional hazards models to measure the association between AG levels and 30-day, 90-day, and 365-day mortality in patients with AKI. Results. A total of 11,573 eligible subjects were extracted from the MIMIC-III. The relationship between AG levels and 30-day all-cause mortality in patients with AKI was nonlinear, with a U-shaped curve. In multivariate analysis, after adjusting for potential confounders, higher AG was a significant predictor of 30-day, 90-day, and 365-day all-cause mortality compared with lower AG (HR, 95% CI: 1.54, 1.33–1.75; 1.55, 1.38–1.73; 1.46, 1.31–1.60). Conclusions. The relationship between AG levels and 30-day all-cause mortality described a U-shaped curve. High-AG levels were associated with increased risk 30-day, 90-day, and 365-day all-cause mortality in critically ill patients with AKI.

Background. There is no evidence to suggest the predictive power of neutrophil percentage-to-albumin ratio (NPAR) in patients with acute kidney injury (AKI). We hypothesized that NPAR would correlate with all-cause mortality in critically ill patients with AKI. Methods. From the MIMIC-III V1.4 database, we extracted demographics, vital signs, comorbidities, laboratory tests, and other clinical data. The clinical endpoints were 30-, 90- and 365-day all-cause mortality in critically ill patients with AKI. Cox proportional hazards models were used to evaluate the prognostic values of NPAR, and subgroup analyses were performed to measure mortality across various subgroups. Results. A total of 7,481 eligible subjects were enrolled. In multivariate analysis, after adjustments for age, ethnicity, gender, and other confounding factors, higher NPARs were associated with an increased risk of 30-, 90- and 365-day all-cause mortality in critically ill patients with AKI (tertile 3 versus tertile 1: adjusted HR, 95% CI: 1.48, 1.30–1.69; 1.47, 1.31–1.66; 1.46, 1.32–1.62, respectively; P trend <0.01). A similar trend was observed in the NPAR group division by quintiles. Subgroup analysis revealed no significant interactions in most strata. Conclusions. Increased NPAR correlates with increased risk of all-cause mortality in critically ill patients with AKI.

Background Several investigators have sought risk factors for mortality in acute kidney injury (AKI). However, no epidemiological studies have investigated the impact of red blood cell distribution width (RDW) on prognosis for critically ill patients with AKI. The aim of this study was to investigate the association of RDW with mortality in these patients. Methods We analyzed data from the MIMIC-III. RDW was measured upon ICU admission. The association between RDW and mortality of AKI was determined using a multivariate logistic regression and was expressed as the adjusted odds ratio with associated 95% confidence interval (CI). We also conducted subgroup analyses to determine the consistency of this association. Results A total of 14,078 critically ill patients with AKI were eligible for this analysis. In multivariate analysis, adjusted for age and gender and compared with the reference group (RDW 11.1-13.4%) related to hospital mortality, the adjusted ORs (95% CIs) for RDW levels 13.5-14.3%, 14.4-15.6%, and 15.7-21.2% were 1.22 (1.05, 1.43), 1.56 (1.35, 1.81), and 2.66 (2.31, 3.06), respectively. After adjusting for confounding factors, with high RDW linked to an increase in mortality (RDW 15.7-21.2% versus 11.1-13.4%: OR, 1.57; 95% CI, 1.22 to 2.01; P trend <0.0001). A similar trend was observed for 30-day mortality. Conclusions RDW appeared to be an independent prognostic marker in critically ill patients with AKI and higher RDW was associated with increased risk of mortality in these patients.

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