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Introduction Pancreatic portal hypertension (PPH) is a rare complication of acute pancreatitis (AP) that can lead to severe gastrointestinal bleeding. The risk factors associated with PPH, as well as the overall prognosis, warrant further investigation. This study aims to develop and validate a nomogram to predict PPH in patients with AP.Methods Consecutive patients with AP from 2015 to 2023 were retrospectively included in the study. Demographic data, clinical manifestations within the first week of AP onset, and initial contrast-enhanced CT findings were used to develop the predictive model. Univariate and multivariate Cox regression analyses were performed to identify risk factors for PPH. Based on the results of the multivariate analysis, a nomogram was developed. The patients were randomly divided into training and validation sets at a 7:3 ratio. The accuracy and discriminative power of the predictive model were assessed using the area under the curve (AUC) from the receiver operating characteristic curve and the calibration curve.Results Of the 1473 patients with AP, 107 (7.3%) developed PPH within 6 months (range: 2–22 months) during follow-up. Multivariate regression analysis showed that body mass index (BMI) (HR, 1.10; 95% CI 1.04 to 1.16; p=0.001), moderately severe grade (HR, 9.36; 95% CI 4.58 to 19.13; p

Abstract In recent years, the environmental health issue of microplastics has aroused an increasingly significant concern. Some studies suggested that exposure to polystyrene microplastics (PS-MPs) may lead to renal inflammation and oxidative stress in animals. However, little is known about the essential effects of PS-MPs with high-fat diet (HFD) on renal development and microenvironment. In this study, we provided the single-cell transcriptomic landscape of the kidney microenvironment induced by PS-MPs and HFD in mouse models by unbiased single-cell RNA sequencing (scRNA-seq). The kidney injury cell atlases in mice were evaluated after continued PS-MPs exposure, or HFD treated for 35 days. Results showed that PS-MPs plus HFD treatment aggravated the kidney injury and profibrotic microenvironment, reshaping mouse kidney cellular components. First, we found that PS-MPs plus HFD treatment acted on extracellular matrix organization of renal epithelial cells, specifically the proximal and distal convoluted tubule cells, to inhibit renal development and induce ROS-driven carcinogenesis. Second, PS-MPs plus HFD treatment induced activated PI3K-Akt, MAPK, and IL-17 signaling pathways in endothelial cells. Besides, PS-MPs plus HFD treatment markedly increased the proportions of CD8+ effector T cells and proliferating T cells. Notably, mononuclear phagocytes exhibited substantial remodeling and enriched in oxidative phosphorylation and chemical carcinogenesis pathways after PS-MPs plus HFD treatment, typified by alterations tissue-resident M2-like PF4+ macrophages. Multispectral immunofluorescence and immunohistochemistry identified PF4+ macrophages in clear cell renal cell carcinoma (ccRCC) and adjacent normal tissues, indicating that activate PF4+ macrophages might regulate the profibrotic and pro-tumorigenic microenvironment after renal injury. In conclusion, this study first systematically revealed molecular variation of renal cells and immune cells in mice kidney microenvironment induced by PS-MPs and HFD with the scRNA-seq approach, which provided a molecular basis for decoding the effects of PS-MPs on genitourinary injury and understanding their potential profibrotic and carcinogenesis in mammals. Graphical Abstract