Acute kidney injury (AKI) is a common early complication in critically ill burn patients, but its risk factors remain incompletely understood. This study aimed to identify independent risk factors for early AKI in this population. A retrospective study enrolled 98 critically ill burn patients admitted to the participating medical center from January 2016 to September 2025. Patients were divided into AKI and non-AKI groups based on AKI occurrence within 3 days post-injury. Admission data (demographics, laboratory parameters, inflammatory indices) were analyzed. Independent risk factors were identified via univariate analysis, multicollinearity diagnosis, and multivariate logistic regression; a prediction model was constructed and evaluated using ROC curve analysis. The incidence of early AKI in critically ill burn patients was 28.6%. The multivariate logistic regression analysis revealed that blood urea nitrogen (BUN; OR = 1.519; 95% CI: 1.042 ~ 2.214; p = 0.030), cystatin C (CYS; OR = 12.142; 95% CI: 1.240 ~ 118.858; p = 0.032), and D-dimer (OR = 1.136; 95% CI: 1.006 ~ 1.283; p = 0.040) levels were independent risk factors for early AKI. The prediction model equation was Logit(P) = -9.159 + 0.418 × BUN (mmol/L) + 2.497 × CYS (mg/L) + 0.127 × D-dimer (mg/L). The area under the ROC curve (AUC) for this model was 0.887 (95% CI: 0.816 ~ 0.958; p < 0.001), and the optimal cut-off value was determined by the maximum Youden index, which was 0.235. According to the prediction equation, a calculated probability p ≥ .235 indicates a high risk of early AKI. Elevated BUN, CYS, and D-dimer levels increase early AKI risk in critically ill burn patients.

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease in which environmental and medication-related exposures may precipitate disease onset or flares in susceptible individuals, which can result in lupus nephritis (LN) and, in rare cases, posterior reversible encephalopathy syndrome (PRES). Immediate hypersensitivity reactions preceding the initial presentation of SLE have rarely been described. We report that a 21-year-old Hispanic woman developed airway-compromising angioedema, encephalopathy, and generalized tonic-clonic seizures, requiring intubation after her first depot medroxyprogesterone acetate (DMPA) injection. Brain magnetic resonance imaging (MRI) demonstrated PRES with extensive posterior vasogenic edema consistent with PRES with hemorrhagic transformation and bilateral posterior cerebral artery vasoconstriction. Laboratory evaluation revealed acute kidney injury with proteinuria, hypocomplementemia, positive antinuclear and antidouble-stranded DNA antibodies, and positive SSA antibodies. Kidney biopsy confirmed class IV diffuse LN. Treatment included pulse corticosteroids, seizure prophylaxis, immunosuppressants, and antihypertensive therapy, resulting in neurological and renal recovery. Although causality cannot be inferred, the temporal sequence raises the hypothesis that immune activation associated with DMPA exposure, or hypersensitivity to one of its excipients, may have contributed to the clinical unmasking of autoimmune disease.

Hantavirus infection is an uncommon but potentially life-threatening zoonotic disease that requires early recognition in the emergency department. This letter summarizes the epidemiology, transmission, clinical manifestations, diagnostic approaches, and current management of hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS). Although the initial presentation is often nonspecific, rapid progression to respiratory failure, shock, or acute kidney injury may occur, necessitating prompt diagnosis and aggressive supportive care. Serologic testing remains the primary diagnostic modality, while treatment is largely supportive, with extracorporeal membrane oxygenation reserved for selected patients with severe HPS. Increased awareness among emergency physicians and timely implementation of infection-control measures are essential to improve patient outcomes and reduce mortality.

Quercus laurina is an oak species used orally in Mexican folk medicine. However, its toxicological profile has not yet been evaluated, which makes it difficult to determine safe doses for traditional preparations. This study, for the first time, evaluates the acute toxicity of an ethanolic extract of Q. laurina bark (QLBE) in Wistar rats in accordance with OECD guideline 423, and it explores the impact of QLBE on mitochondrial bioenergetics and glycolytic capacity in primary hepatocytes to determine whether the extract alters cellular energy metabolism. QLBE at 2000 mg/kg elicited death and tremors, and a dose-dependent hepatic injury, in addition to histopathological changes in the kidney, brain, lung, and heart. QLBE caused a significant reduction in the basal, ATP-linked, spare, and maximal mitochondrial respiratory capacities of hepatocytes, and it decreased glycolytic capacity after 2 and 24 h of exposure. These findings indicate that QLBE disrupts mitochondrial bioenergetics and glycolytic activity in hepatocytes, alterations that may be associated with the observed liver toxicity. HPLC and GC-MS analyses identified myo-inositol, quininic acid, and ellagic acid as the primary metabolites of QLBE. The results demonstrated the toxic potential of QLBE, thereby discouraging its unregulated use in traditional remedies in Mexican folk medicine.

Cisplatin-induced acute kidney injury (AKI) is a dose-limiting chemotherapy complication laking effective clinical interventions. This study investigated the protective mechanisms of proanthocyanidins (PACs), a promising food-derived polyphenol, against cisplatin-induced systemic toxicity in C57BL/6 mice. Multi-omics integration combining 16S rRNA sequencing and renal transcriptomics, was employed to identify microbial-metabolic signaling nodes. Notably, 7-day PAC pretreatment (25 or 50 mg/kg/day) significantly alleviated renal dysfunction, normalized serum creatinine, blood urea nitrogen, reinforced renal antioxidant defenses, and suppressed kidney inflammation. Transcriptomic profiling revealed that cisplatin-induced renal damage was associated with the dysregulation of the cAMP signaling pathway, which was effectively reversed by PACs. Furthermore, 16S rRNA sequencing revealed that PACs restructured the gut microbiota by suppressing the pathogenic taxa (Alistipes and CAG_485) and enriching beneficial taxa (Muribaculaceae). Integrated network analysis further linked these microbial shifts to the stabilization of renal cAMP signaling and redox homeostasis, suggesting a coordinated gut-kidney crosstalk. In conclusion, PACs function as a multifaceted food-derived adjuvant that potentially attenuates cisplatin-induced AKI, providing a molecular framework for gut-targeted nutritional intervention in chemotherapy-induced systemic toxicity.