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Background The renal angina index (RAI) is a useful tool for risk stratification of acute kidney injury (AKI) in critically ill children. We evaluated the performance of a modified adult RAI (mRAI) for the risk stratification of AKI in critically ill adults. Methods We used two independent intensive care unit (ICU) cohorts: 13   965 adult patients from the University of Kentucky (UKY) and 4789 from University of Texas Southwestern (UTSW). The mRAI included: diabetes, presence of sepsis, mechanical ventilation, pressor/inotrope use, percentage change in serum creatinine (SCr) in reference to admission SCr (ΔSCr) and fluid overload percentage within the first day of ICU admission. The primary outcome was AKI Stage ≥2 at Days 2–7. Performance and reclassification metrics were determined for the mRAI score compared with ΔSCr alone. Results The mRAI score outperformed ΔSCr and readjusted probabilities to predict AKI Stage ≥2 at Days 2–7: C-statistic: UKY 0.781 versus 0.708 [integrated discrimination improvement (IDI) 2.2%] and UTSW 0.766 versus 0.696 (IDI 1.8%) (P   <   0.001 for both). In the UKY cohort, only 3.3% of patients with mRAI score <10 had the AKI event, while 16.4% of patients with mRAI score of ≥10 had the AKI event (negative predictive value 96.8%). Similar findings were observed in the UTSW cohort as part of external validation. Conclusions In critically ill adults, the adult mRAI score determined within the first day of ICU admission outperformed changes in SCr for the prediction of AKI Stage ≥2 at Days 2–7 of ICU stay. The mRAI is a feasible tool for AKI risk stratification in adult patients in the ICU. [ABSTRACT FROM AUTHOR]

Elevated plasma levels of plasminogen activator inhibitor‐1 (PAI‐1) are documented in patients with sepsis and levels positively correlate with disease severity and mortality. Our previous work demonstrated that visceral adipose tissues (VAT) are a major source of PAI‐1, especially in the aged (murine endotoxemia), that circulating PAI‐1 protein levels match the trajectory of PAI‐1 transcript levels in VAT (clinical sepsis), and that PAI‐1 in both VAT and plasma are positively associated with acute kidney injury (AKI) in septic patients. In the current study utilizing preclinical sepsis models, PAI‐1 tissue distribution was examined and cellular sources, as well as mechanisms mediating PAI‐1 induction in VAT, were identified. In aged mice with sepsis, PAI‐1 gene expression was significantly higher in VAT than in other major organs. VAT PAI‐1 gene expression correlated with PAI‐1 protein levels in both VAT and plasma. Moreover, VAT and plasma levels of PAI‐1 were positively associated with AKI markers, modeling our previous clinical data. Using explant cultures of VAT, we determined that PAI‐1 is secreted robustly in response to recombinant transforming growth factor β (TGFβ) and tumor necrosis factor α (TNFα) treatment; however, neutralization was effective only for TNFα indicating that TGFβ is not an endogenous modulator of PAI‐1. Within VAT, TNFα was localized to neutrophils and macrophages. PAI‐1 protein levels were fourfold higher in stromal vascular fraction (SVF) cells compared with mature adipocytes, and among SVF cells, both immune and nonimmune compartments expressed PAI‐1 in a similar fashion. PAI‐1 was localized predominantly to macrophages within the immune compartment and preadipocytes and endothelial cells within the nonimmune compartment. Collectively, these results indicate that induction and secretion of PAI‐1 from VAT is facilitated by a complex interaction among immune and nonimmune cells. As circulating PAI‐1 contributes to AKI in sepsis, understanding PAI‐1 regulation in VAT could yield novel strategies for reducing systemic consequences of PAI‐1 overproduction. [ABSTRACT FROM AUTHOR]

Objectives/Hypothesis: To better assess rates of postoperative complications and mortality following esophageal dilation, and to identify factors associated with adverse outcomes. Study Design: Observational, retrospective cohort study. Methods: We queried a national database of insurance claims for Current Procedural Terminology (CPT) codes representing esophageal dilation performed between 2011 and 2017. Patients aged 18 to 100 who were continuously enrolled with their insurance provider were included. Demographic information, additional CPT codes, concomitant diagnoses, and anticoagulant medication data were collected for all patients included. Postoperative mortality was assessed and International Classification of Diseases (ICD)9/10 codes for complications, including esophageal perforation, hemorrhage, mediastinitis, and sepsis were flagged. Results: We identified 202,965 encounters for esophageal dilation. Of these procedures, 193 were performed on a patient who underwent percutaneous endoscopic gastrostomy (PEG) during the study period and was analyzed separately. Another 244 dilations were excluded due to repeat entries. Of the remaining 202,528 procedures remaining, 42,310 were repeat dilations in the same patient. Data analysis was confined to each patient's initial dilation. 160,218 initial dilations remained. Of these, 62,107 were performed on male patients and 98,111 were performed on female patients. The average age was 57.7 years. There were 12 mortalities within 30 days postoperatively, representing 0.0075% of all dilations. Esophageal perforation and esophageal hemorrhage were the most common reported complications, with 139 and 110 occurrences, respectively. The overall per‐dilation complication rate was 0.215%. Conclusions: Evidence from a national insurance claim database suggests that esophageal dilation is a safe procedure with a low rate of serious complications and a 30‐day all‐cause mortality rate of less than 1 per 10,000 dilations. Level of Evidence: 4 Laryngoscope, 131:2436–2440, 2021 [ABSTRACT FROM AUTHOR]