Introduction Most CKD patients experience cardiovascular issues before commencing renal replacement therapy. An accuracy prediction model is helpful for physicians to assess cardiovascular prognoses in each individual, and to provide insights on how to outline individualized lines of therapy. Method This study enrolled 1138 participants with non-dialysis-dependent chronic kidney disease (NDD-CKD). Following a proportion of 7:3, patients were randomly assigned to training and validation cohorts. The relevant predictors of cardiovascular events were screened using the least absolute shrinkage and selection operator (Lasso) regression. The area under the receiver operating characteristic curve (AUC) and the calibration curve with 1000 bootstraps resamples were used to assess the nomogram's performance. Tests on the discrimination of the prediction model used Kaplan-Meier (KM) curve. Results After screening all the predictors by lasso regression, the five remaining ones (albumin, estimated glomerular filtration rate, etiology of CKD, cardiovascular disease history, and age) were used to construct the prediction model. The AUC of 1-year, 2-year, and 3-year was 0.81 (95% CI = 0.75–0.87), 0.80 (95% CI = 0.75–0.86), and 0.80 (95% CI = 0.73–0.86), respectively. The calibration curve and the KM curve showed good prediction features, and the external validation also had a good prediction performance (AUC of 1-, 2-, and 3-years were 0.77, 0.84, and 0.82, respectively). Conclusion We successfully developed a novel nomogram that has decent prediction performance and can be used for assessing the probability of cardiovascular events in patients with NDD-CKD, displaying valuable potential for clinical application.

Ferroptosis is implicated in the progression of ulcerative colitis (UC), and interferon regulatory factor 7 (IRF7) contributes to cell death. This study probed the mechanism of IRF7 in ferroptosis of colonic epithelial cells (ECs) in mice with dextran sodium sulfate (DSS)-induced UC. The UC mouse model and the in vitro ferroptosis model were respectively established by DSS feeding and the treatment of FIN56 (a ferroptosis inducer). Results of quantitative real-time polymerase chain reaction and western blotting revealed the upregulation of IRF7 and solute carrier family 11 member 2 (SLC11A2/NRAMP2/DMT1) and the downregulation of microRNA (miR)-375-3p in DSS-treated mice and FIN56-treated ECs. Silencing of IRF7 improved the symptoms of UC in DSS-induced mice and decreased the levels of tumor necrosis factor α, interleukin 6, monocyte chemoattractant protein 1, and interleukin 1β, reactive oxygen species, iron ions, lipid peroxidation, and increased glutathione and glutathione peroxidase 4. Chromatin immunoprecipitation and dual-luciferase assays showed that binding of IRF7 to the miR-375-3p promoter inhibited miR-375-3p expression, and miR-375-3p suppressed SLC11A2 transcription. The rescue experiments revealed that knockdown of miR-375-3p neutralized the role of silencing IRF7 in alleviating ferroptosis of colonic ECs. Overall, IRF7 upregulated SLC11A2 transcription by inhibiting miR-375-3p expression, thereby prompting ferroptosis of colonic ECs and UC progression in DSS-treated mice.