Chronic kidney disease (CKD) is a progressive condition, often silent until advanced stages. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) reduce hyperfiltration, albuminuria, and inflammation, slowing CKD progression. Although landmark trials demonstrated such benefits between 2015 and 2024, guideline adoption for cardio-renal protection evolved between 2020 and 2024, resulting in variable real-world implementation during this period. We conducted a retrospective electronic health record-based analysis using the UCLA i2b2 database from 2016 to 2026 to evaluate utilization of these therapies among CKD patients. Outcomes were stratified by sex, race, ethnicity, and age, with progression to ESKD as the primary outcome. Among 77,911 patients, 7.0% had observed progression to ESKD. Patients receiving SGLT2i had lower observed progression rates compared to non-users (5.9% vs 7.1%, 16% reduction), with similar reductions in those receiving either therapy class. Females had lower utilization than males for SGLT2i (6.1% vs 8.9%) and GLP-1RA (3.8% vs 4.2%), yet observed differences were greater among them (observed relative risk reduction (RRR) female 26% vs male 15%). Similar outcomes were observed among Hispanic and Latino patients (observed RRR 31%), White patients (observed RRR 24%), and those aged 55-64 years (observed RRR 32%). These findings reveal an ongoing guideline-to-practice gap, highlighting the need for equitable and timely use of nephroprotective therapies.

Background/Purpose: GLP‑1 receptor agonists (GLP‑1 RAs) like semaglutide and liraglutide offer cardiovascular and metabolic benefits, but their perioperative potential in cardiopulmonary bypass (CPB) surgery is understudied. Understanding agent-specific effects on metabolic stress, inflammation, and cardiac function could inform strategies to improve recovery. Objectives: To systematically review evidence on GLP‑1 RAs relevant to CPB, comparing mechanisms, metabolic effects, cardiovascular outcomes, perioperative glucose control, and implications for surgical recovery. Methods: PubMed, Scopus, and MEDLINE were searched through early 2026 for trials, reviews, and perioperative studies of GLP‑1 RAs. Data on pharmacology, cardiovascular outcomes, glycemic control, and perioperative effects were extracted. Results: GLP‑1 RAs reduce major adverse cardiovascular events, mortality, and improve glycemic and inflammatory profiles. Semaglutide shows longer half-life and stronger weight and glucose effects; liraglutide enhances insulin secretion and perioperative glycemic control. Limited CPB-specific data suggest metabolic stabilization, though broad clinical benefits remain unproven. Conclusions: Evidence supports the hypothesis that semaglutide and liraglutide could enhance postoperative outcomes via metabolic and cardioprotective effects. Prospective CPB-focused trials are needed to clarify comparative efficacy, optimal agent selection, and mechanistic pathways.

Most commonly found in sensory and sympathetic ganglia neurons, Nav 1.7 channels are a subset of voltage-gated sodium channels that are sensitive to reactive oxygen species (ROS). This property has been most widely studied in nociception where increased ROS levels, such as in conditions like optic neuropathies, are an indicator of tissue damage and as such, pain. Within optic neuropathies, a small subset of retinal ganglion cells known as intrinsically photosensitive retinal ganglion cells (ipRGCs) preferentially survive and uniquely express high levels of Na 1.7 RNA. It is unknown if this higher expression translates to the protein level and could serve as a mechanism for the ipRGCs to respond to high ROS levels. Our hypothesis is that Nav 1.7 staining will be seen in the cell membranes of ipRGCs in wild type mice. In our investigation, our data was not supportive of this hypothesis. Nav 1.7 staining was not seen in the RGC layer or the ipRGCs themselves. These findings indicate that Nav 1.7 protein is not expressed in WT mice, potentially suggesting a mechanism that Nav 1.7 is induced by certain disease states with high ROS content. Therefore, our future testing will use mouse models such as the RD10 and OPA1 knockout mice to retest this hypothesis of Nav 1.7 expression in the context of high ROS states.

Background: Acetaminophen (APAP) is a leading cause of pediatric acute liver failure. Adult derived prognostic tools like the King’s College Criteria (KCC) may fail to identify children at risk of severe hepatotoxicity, disability, or death. Objective: To describe the clinical presentation of pediatric APAP induced liver injury and assess KCC’s prognostic value in children. Methods: We performed a multicenter (6 sites) observational study of confirmed APAP induced liver injury in children aged 5 months to 17 years from 2015 to 2023. Chart review captured demographics, ingestion/treatment features, and laboratory values. Outcome was categorized as full recovery or a poor composite outcome (transplant, disability or death). Data are stratified by age 0-7 years and 8-17 years. Results: Of 204 total patients, 16 (7.8%) were aged 0-7 and 188 (92.1%) were 8-17. Poor composite outcomes occurred in 4 (25%) of the 0-7 vs. 8 (4.2%) of the 8-17 age group. Delays to presentation and/or treatment, and severe peak lab values were more common in those with poor composite outcomes. The KCC was met by 26 (12.7%) patients, 20 (76.9%) of whom fully recovered. For patients aged 0-17, KCC sensitivity for the composite outcome was 0.833 (CI 0.516-0.979) and specificity was 0.916 (CI 0.868-0.951). Conclusions: Children ages 0 to 7 had disproportionately worse outcomes than those 8 to 17, suggesting potential age-related vulnerability after severe injury. KCC’s limited diagnostic performance highlights its limitations in predicting pediatric mortal

Opioids remain the primary analgesics used during surgical procedures, however their use can lead to adverse effects, including nausea, respiratory depression, postoperative hyperalgesia, and increased risk for chronic abuse liability. Identifying non-opioid-based anesthetic strategies that adequately control surgical pain represents a promising alternative to improve quality of recovery (QoR). Dexmedetomidine, an α2-adrenergic receptor agonist with analgesic properties, has been suggested as a potential alternative to traditional opioid-based anesthesia (OBA), but preclinical models assessing dexmedetomidine QoR benefits over opioids remain limited. In this study, we used preclinical models (mice) and combined behavioral and cytokine analysis to investigate the benefits/costs of Opioid Free Anesthesia (OFA) versus OBA on intra- and post-operative outcomes. To investigate fluctuations in inflammatory biomarkers as a function of drug regimen, we collected blood from animals and conducted a battery of behavioral models to assess ongoing pain in mice before, 1, 2, 3, and 7 days after laparotomy. Our results uncover the presence of post-operative pain and allowed us to establish a QoR recovery score in non-verbal mammals (mice). The findings of our study demonstrate no significant difference in inflammatory biomarker and behavioral outcomes between OFA and OBA. This work represents a stepping stone in better defining ongoing pain during postoperative settings and an improved tool to refine pharmaceutical treatment of pain.