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.

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.

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Oral propionate activated vagal afferent nerve in the gut and facilitated solitary nucleus in the brain via nodose ganglia to activate vagal efferent nerve innervating the heart, so as to reduce ventricular arrhythmia after myocardial infarction.