Background: Contrast media (CM) is widely used in cardiac catheterization; however, it may cause contrast-induced acute kidney injury (CI-AKI) which severely increases mortality. MicroRNA (miRNA) has been found to participate in the process of acute kidney injury (AKI), and this discovery has great potential for diagnosis and treatment. However, the role of miRNA in CI-AKI is still unclear. This study aimed to investigate the regulatory effect miRNAs exert in CI-AKI.Methods: We established a novel, representative, isotonic CI-AKI model by using CM iodixanol, a CM which is commonly used in clinic. Next-generation sequencing and reverse transcription polymerase chain reaction (RT-qPCR) were performed to determine the expression of miRNA-188 in CI-AKI. Western blot analysis of the apoptosis regulator protein and TUNEL assay were ordered to evaluate apoptosis.Bioinformatics and double luciferin reporter gene assay were performed to predict and to confirm the interaction between microRNA-188 and SRSF7. Results:The novel isotonic CI-AKI rat model we established exhibited typical characteristics of CI-AKI in serum creatinine, cystatin C, HE staining, and under electron microscope observation. Sequencing and RT-qPCR demonstrated that miRNA-188 was significantly up-regulated both in CI-AKI rat and HK-2 cell models while overexpression of miRNA-188 significantly aggravated apoptosis in CI-AKI cell models. SRSF7 was identified as a direct target gene of miRNA-188, and dual luciferase reporter assay determined the direct interaction between SRSF7 and miRNA-188. In addition, SRSF7 silencing reduced the cell viability rate of the CI-AKI cell model. Conclusions:The present study's findings indicate that miRNA-188 aggravated contrast-induced apoptosis by regulating SRSF7, which may serve as a potential drug target for CI-AKI intervention.
Background: Risk stratification is recommended as the key step to prevent contrast-associated acute kidney injury (CA-AKI) among at-risk patients following coronary angiography (CAG) and/or percutaneous coronary intervention (PCI). Patients with hypoalbuminemia are prone to CA-AKI and do not have their own risk stratification tool. Therefore, this study developed and validated a new model for predicting CA-AKI among hypoalbuminemia patients CAG/PCI. Methods: 1272 patients with hypoalbuminemia receiving CAG/PCI were enrolled and randomly allocated (2:1 ratio) into the development cohort (n = 848) and the validation cohort (n = 424). CA-AKI was defined as an increase of ≥0.3 mg/dL or 50% in serum creatinine (SCr) compared to baseline in the 48 to 72 h after CAG/PCI. A prediction model was established with independent predictors according to stepwise logistic regression, showing as a nomogram. The discrimination of the new model was evaluated by the area under the curve (AUC) and was compared to the classic Mehran CA-AKI model. The Hosmer-Lemeshow test was conducted to assess the calibration of our model. Results: Overall, 8.4% (71/848) patients of the development group and 11.2% (48/424) patients of the validation group experienced CA-AKI. A new nomogram included estimated glomerular filtration rate (eGFR), serum albumin (ALB), age and the use of intra-aortic balloon pump (IABP); showed better predictive ability than the Mehran score (C-index 0.756 vs. 0.693, p = 0.02); and had good calibration (Hosmer-Lemeshow test p = 0.187). Conclusions: We developed a simple model for predicting CA-AKI among patients with hypoalbuminemia undergoing CAG/PCI, but our findings need validating externally. Trial registration: http://www.ClinicalTrials.gov NCT01400295, retrospectively registered 21 July 2011.
ObjectiveSeveral studies evaluating the preventive effect of N-acetylcysteine (NAC) on contrast-associated acute kidney injury (CA-AKI) among patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI) have suggested inconsistent results and that a systematic review and meta-analysis should be performed.DesignSystematic review and meta-analysis.Data sourcesPubMed, MEDLINE, EMBASE, ClinicalTrials.gov and the Cochrane Central databases were searched from inception to 15 November 2019.Eligibility criteriaRandomised controlled trials assessing use of NAC compared with non-use of NAC (eg, placebo) in preventing CA-AKI in patients with STEMI following PPCI were included.Data synthesisRelative risks with 95% CIs were pooled using a random-effects model. Evidence level of conclusions was assessed by Cochrane GRADE measure.ResultsSeven trials including 1710 patients were identified. Compared with non-use of NAC, use of NAC significantly reduced the incidence of CA-AKI by 49% (risk ratio (RR) 0.51, 95% CI 0.31 to 0.82, p<0.01) and all-cause in-hospital mortality by 63% (RR 0.37, 95% CI 0.17 to 0.79, p=0.01). The estimated effects on the requirement for dialysis (RR 0.61, 95% CI 0.11 to 3.38, p=0.24) were not statistically significant. Trial sequential analysis confirmed the true positive of NAC in reducing risk of CA-AKI. Subgroup analyses suggested that the administration of NAC had greater benefits in patients with renal dysfunction and in those receiving oral administration and higher dosage of NAC.ConclusionsNAC intake reduces the risk of CA-AKI and all-cause in-hospital mortality in patients with STEMI undergoing PPCI. The estimated potential benefit of NAC in preventing dialysis was ambiguous, and further high-quality studies are needed.PROSPERO registration numberCRD42020155265.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.