Background: Contrast-induced acute kidney injury (CI-AKI) is considered to be the third leading cause of hospital-acquired kidney injury. Current studies mostly suggest that contrast agents mainly harm renal tubular epithelial cells, but we hypothesized that the development of CI-AKI should be the result of the interaction of renal vascular and tubular injury. Methods: First we constructed a CI-AKI mouse model and verified the success of the model by pathological injury and serum creatinine level. Immunohistochemistry, protein quantification and qRT-PCR were used to detect the location and level of expression of neutrophil extracellular traps (NETs) in the kidney. Then, we blocked the in vivo accumulation of NETs using GSK484 and DNase I and detected the expression of NETs and the damage of glomerular and peritubular capillaries. Results: We first identified the presence of NETs in CI-AKI mice, and NETs were mainly accumulated in glomeruli and peritubular capillaries. The expression of NETs was positively correlated with the severity of CI-AKI kidney. After inhibition of NETs release or promotion of NETs degradation by drugs, renal vascular endothelial cell injury was reduced and renal pathological changes and creatinine levels were reversed in CI-AKI mice. In addition, inhibition of NETs reduced apoptosis and pyroptosis of renal cells and attenuated inflammation in vivo. Conclusion: These findings suggest that NETs are involved in the development of CI-AKI by damaging glomerular and peritubular capillary endothelial cells. This study will provide a new strategy for clinical prevention and treatment of CI-AKI.

Abdominal aortic aneurysms (AAA) are a significant health concern in developed countries due to their considerable mortality rate. The crucial factor of the progression of AAA is the release of neutrophils and neutrophil extracellular traps (NETs). Magnetic particle imaging (MPI) is a new imaging technique that offers the capability to detect superparamagnetic iron oxide nanoparticles (SPION) with exceptional sensitivity. We aimed to investigate the functional imaging of MPI for the detection and monitoring of neutrophil infiltration within AAA. A novel multimodal imaging agent targeting neutrophils, PEG-Fe₃O₄-Ly6G–Cy7 nanoparticles (Ly6G NPs), were designed by coupling Fe₃O₄ nanoparticles with Ly6G antibodies and Cy7. The targeting and sensitivity of Ly6G NPs were assessed using MPI and fluorescence imaging (FLI) in the AAA mouse model. After the inhibition of NETosis, the degree of neutrophil infiltration and AAA severity were assessed using MPI with Ly6G NPs. Ly6G NPs accurately localized and quantitatively analyzed AAA lesion sites in mice using MPI/FLI/CT. Compared to the control group, elevated MPI and FLI signal intensities were detected at the abdominal aortic lesion site, and neutrophil infiltration and NETs accumulation were detected by histological analysis in the AAA models. After the inhibition of NETs accumulation in vivo, pathological damage in the abdominal aorta was significantly reduced, along with a decrease in the accumulation of Ly6G NPs and MPI signals. This multimodal MPI strategy revealed that nanoparticles targeting Ly6G can be used to detect neutrophil infiltration within AAA and monitor AAA severity.

Background: Chronic kidney disease is a major global health concern, with type 2 diabetic nephropathy (T2DN) significantly contributing to its burden. This study examines global trends, key risk factors, and clinical characteristics of T2DN to identify modifiable contributors and inform precision management. Methods: Data from the 2021 GBD Study, Mendelian randomization (MR) analyses, NHANES, and a clinical cohort were utilized. Trends in prevalence, incidence, mortality, disability-adjusted life years (DALYs), and population-attributable fractions (PAF) of T2DN risk factors were analyzed globally and across sociodemographic strata. Genetic determinants were identified via two-sample and multivariable MR, while clinical data were analyzed using regression and correlation analyses. Results: Between 1990 and 2021, T2DN prevalence, incidence, and DALYs increased globally, and the global mortality rate rose from 5.73 (4.81, 6.83) to 10.25 (8.62, 12.15). High fasting plasma glucose was the primary risk factor, with rising PAFs for high BMI and systolic blood pressure (SBP), and the global PAF for deaths due to T2DN attributed to high fasting plasma glucose increased from 0.80 to 0.90. MR analysis confirmed causal links between fasting glucose (β = 1.351, P = 2.78e− 4), insulin (β = 2.543, P = 1.20e− 5), T2DM (OR = 2.280, P = 4.14e− 29) and T2DN risk, with BMI and SBP influencing disease progression. NHANES data showed BP’s impact on renal function. A diagnostic model incorporating age, categorical blood pressure data, history of heart failure, and history of stroke was developed, with an AUC of 0.716. In the clinical cohort, T2DN correlated with elevated urinary albumin-to-creatinine ratio, serum creatinine, BP, and BMI variations. Conclusion: T2DM progression to T2DN is driven by hyperglycemia, BMI, and BP, highlighting the need for targeted interventions.

Aortic dissection (AD) is a life-threatening aortic emergency that progresses rapidly and carries a high mortality rate. We characterised contemporary patterns and long-term trends in AD mortality in the United States and examined associations between ambient temperature and AD mortality. We obtained mortality data for AD from United States CDC WONDER for 1999–2023 and calculated age-adjusted mortality rates (AAMR). Temporal trends were assessed using Joinpoint regression to estimate annual percent change (APC) and average annual percent change (AAPC). Monthly air temperature data for the period 1999–2023 were obtained from the North America Land Data Assimilation System (NLDAS). Associations between temperature and AD mortality were evaluated across census regions using correlation analyses and Poisson regression models. To explore the future burden, subgroup-specific time series models (ARIMA or ETS) were applied to generate 20-year forecasts. In 2023, there were 4,418 AD deaths (AAMR 1.73 per 100,000; 95% CI 1.68–1.78); rates were highest in the Midwest (1.96), in male (2.19 vs 1.24 in female), in non-Hispanic Black individuals (2.75), and in adults ≥85 years (11.67). From 1999–2023, 86,943 deaths occurred and the overall AAMR declined (AAPC −0.37), but reversed to sustained increases after 2013. Across the four census regions, the monthly AAMR was lowest in summer and highest in winter during 1999–2023 (P < 0.05). A 10°F increase in temperature was associated with lower mortality risk (eg, South RR 0.889). AD mortality has rebounded since 2013 with marked demographic and regional disparities. Lower temperatures and greater thermal variability are linked to higher mortality, supporting seasonally and region-tailored prevention and health-system preparedness.