A 17-month-old neutered male Bedlington terrier weighing 5.4 kg was presented because of vomiting, lethargy, and oliguria. Serum chemistry analysis revealed severe azotemia and ultrasonography revealed hyperechoic renal cortices. Acorn-induced acute kidney injury was suspected based on the animal's history of eating dried acorns over the previous 8 d. The dog did not respond to conventional intravenous fluid therapy, but his condition improved with intermittent hemodialysis. Although acorn intoxication is well documented in grazing animals, including cattle, it has rarely been reported in dogs. Acorns can cause acute kidney or liver injury, with high mortality rates. To the best of our knowledge, this is the first reported canine case of acorn toxicosis successfully treated with hemodialysis. The case findings indicate the importance of raising awareness among pet owners about the potential life-threatening effects of consuming acorns, particularly in regions where animals' exposure to acorns is likely. Key clinical message: Acorn ingestion can cause life-threatening acute kidney injury in dogs. Early recognition and timely intervention with hemodialysis can result in successful outcomes.

We report a 13-year-old boy who presented with acute gastroenteritis complicated by severe dehydration and shock, acute kidney injury (AKI), and encephalopathy caused by Salmonella enterica serovar Weltevreden (S. Weltevreden). Twenty-four hours after admission, the patient developed a cough, and nasopharyngeal reverse transcription polymerase chain reaction (RT-PCR) detected influenza A. However, there was no respiratory distress or tachypnea, and chest radiography was normal. This co-infection likely did not contribute to the severity of illness attributed to S. Weltevreden. The patient improved with prompt fluid resuscitation and intravenous ceftriaxone therapy and recovered completely. Non-typhoidal Salmonella infections remain clinically important because of the potential for severe disease and the growing threat of antimicrobial resistance.

Necrotizing pancreatitis (NP) is a severe and potentially life-threatening complication of acute pancreatitis (AP). This case report discusses NP in a 39-year-old male patient with severe hypertriglyceridemia (HTG), highlighting management and treatment with supportive measures, intravenous insulin, antibiotic use, and total parenteral nutrition (TPN). Despite episodes of hypoglycemia requiring discontinuation of insulin, his triglyceride (TG) levels steadily declined without the need for plasmapheresis or surgical intervention. However, the pancreatitis worsened, leading to circulatory shock due to the acute inflammatory effect of NP and acute renal failure. This case emphasizes the importance of timely diagnosis and multidisciplinary supportive care in the successful treatment of HTG-induced NP.

The present review aimed to evaluate the prognostic value of inflammatory biomarkers in patients undergoing endovascular aortic aneurysm repair (EVAR). A systematic review of relevant studies was performed according to PRISMA guidelines. Articles assessing associations of inflammatory biomarkers with the post-EVAR outcomes were considered. After screening, 34 studies were included (7019 patients were reviewed; mean age: 73.6 years; 91.6% were men); 22 different inflammatory biomarkers were identified among the included studies. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and lymphocyte-to-monocyte ratio (LMR) were investigated in 11, 4, and 3 studies, respectively. Nine studies evaluated the post-implantation syndrome (PIS) and examined its role in post-EVAR outcomes. Increased preoperative NLR was associated with all-cause mortality and acute kidney injury after EVAR. NLR was also reported as an independent risk factor for aneurysm sac regression failure. High preoperative PLR and low preoperative LMR were correlated with acute kidney injury and overall mortality, respectively. PIS was associated with a lower type 2 endoleak rate but had no impact on mortality rates. NLR may be a useful predictor for mortality and poor prognosis in EVAR populations. This may have clinical implications in post-EVAR surveillance programs.

Sepsis-related acute kidney injury (SA-AKI) represents a severe complication associated with elevated mortality rates, primarily driven by imbalanced Th17 immune responses and mitochondrial dysfunction. Consequently, there is an urgent need for a versatile nanomaterial that can enhance mitochondrial performance while also exerting anti-inflammatory effects. A synthetically produced nanoenzyme has the potential to address this challenge. In this study, we created a biomimetic nanozyme (BPQDs@Raw264.7@Kim-1) by engineering clusters of black phosphorus quantum dots (BPQDs) that are coated with macrophage membranes and functionalized with kidney injury molecule-1 (Kim-1) for targeted delivery. This nanozyme improves its antioxidant and anti-inflammatory properties by clustering black phosphorus quantum dots, while the stability of the drug is maintained through encapsulation within Raw264.7 cell membranes. The system effectively achieves homologous targeting via external Kim-1 molecules. The objective of this nanozyme is to modulate the SIRT3/RORγt/STAT3 pathway to reduce Th17-driven inflammation and alleviate SA-AKI. In vitro experiments demonstrated that the nanozyme possesses excellent biocompatibility, efficient cellular uptake, and the ability to scavenge reactive oxygen species (ROS) in LPS-stimulated HK-2 cells. It mitigated mitochondrial injury, decreased apoptosis, and lowered the levels of pro-inflammatory cytokines. Mechanistically, the nanozyme's overexpression of SIRT3 inhibited RORγt/STAT3 signaling, resulting in reduced Th17 differentiation and inflammatory cytokine release. Importantly, silencing SIRT3 negated these therapeutic benefits, underscoring its critical role. This research introduces a targeted nanozyme approach that alleviates SA-AKI by simultaneously restoring the mitochondrial balance and suppressing Th17 inflammation through the SIRT3/RORγt/STAT3 pathway, presenting a promising therapeutic strategy for organ injury caused by sepsis.

Acute kidney injury (AKI) is common in patients with acute coronary syndrome (ACS). However, understanding its prevalence, risk factors and prognosis remains incomplete. We identified 21328 patients admitted for chest pain to a regional hospital in 2021; 6685 had confirmed ACS. AKI episodes were identified by the serum creatinine criteria of the Kidney Disease: Improving Global Outcomes (KDIGO) AKI guideline. The rates of recovery and inpatient, 30-day and 90-day mortality rates were analyzed. Multi-variable analysis showed that ACS was independently associated with AKI (adjusted odds ratio [OR] 2.327; 95% confidence interval [CI] 2.130-2.542; p < 0.0001). Subgroup analysis showed that ACS was independently associated with AKI on admission (adjusted OR 2.516, 95% CI 2.305-2.746, p < 0.0001) but not new-onset AKI during hospitalization. Other factors associated with AKI were similar between patients with and without ACS. AKI in patients with ACS had similar rate of recovery as those without ACS (p = 0.4). Multi-variable logistic regression showed that both ACS types in AKI were associated with higher inpatient, 30-day and 90-day mortality rates, and they had a synergistic effect. Other factors associated with inpatient, 30-day and 90-day mortality rates of patients with AKI were similar between patients with and without ACS. We conclude that ACS was associated with a higher incidence of AKI, and the risk was mainly associated with AKI on admission. The recovery rates from AKI were similar between patients with and without ACS, but the presence of AKI and ACS synergistically increased the inpatient, 30-day and 90-day mortality rates.

Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in renal function. Proximal tubule (PT) cells play a central role in AKI. However, the specific populations and states of PT that facilitate repair remain poorly understood. Here, we combine spatial enhanced resolution omics sequencing with single-nucleus RNA sequencing to profile kidney transcriptomes during AKI. We identify an ischemia-reperfusion injury-induced PT subtype, termed proliferative PT, that likely initiates renal regeneration and exhibits a gene expression enriched in mitosis and metabolic processes. Acsm2 is expressed in proliferative PT and is associated with cell cycle progression. Functional studies reveal the protective role of Acsm2 via deficiency and overexpressing mice. Finally, we identify a subcluster of Fibroblast (FIB_C2) that participates in PT repair through cell-cell communication with proliferative PT. Our study provides an integrated high-resolution spatiotemporal atlas of AKI and reveals the important role of Acsm2 in kidney regeneration.