A decrease in renal function that follows intravascular administration of contrast medium (CM) within a few days is reported as contrast-induced acute kidney injury (CI-AKI). In clinical practice, the imaging procedure is frequently deferred when clinicians consider that the renal risks caused by CM outweigh the benefits of enhanced imaging. However, with an in-depth understanding of AKI and contrast medium, scholars have realized that the decrease in renal function after CM is caused by contrast medium factors and noncontrast medium factors (such as anemia and hemodynamic instability). Therefore, acute kidney injury caused by CM has been overestimated in the past. The term "contrast-associated acute kidney injury (CA-AKI)" has been increasingly used to indicate AKI after intravascular administration of contrast medium compared with CI-AKI. CA-AKI can increase the risk of death and chronic kidney disease. However, its pathophysiological mechanism has not been fully elucidated, and the effectiveness of various preventive and therapeutic measures have been questioned. These present challenges for us. In this article, we will review the diagnostic criteria, epidemiology, risk factors, pathophysiological mechanisms and treatment of CA-AKI to provide optimized imaging procedures in clinical practice.
Background Newly, chemo‐preventive technique might be a hopeful advancement in developing countries for treating cancers with the aid of toxic less natural based constituents. Malignancy urges to augment effectual chemo‐preventive agents that are look forward to suppress the tumours which may be stimulated by chewing and smoking of tobacco and over alcohol consumption related with the high prevalence of human oral cancer (OC) patients. Methods In the present research, we examined to assess antioxidants, lipid peroxidation (LPO) and detoxification enzymes levels of anticancer activity of mangiferin on 0.5% 7.12‐dimethylbenz[a]anthracene (DMBA) provoked hamster cheek pouch carcinoma (HCPC). OC on hamster buccal pouch (HBP) was incited by DMBA treatment for thrice per week for over 14 weeks. Results 100% well defined OC establishment with body weight (bw), tumour burden (TB), antioxidant, LPO and liver marker enzymes and also histological changes were observed on DMBA‐challenged buccal pouch carcinoma (BPC) in hamsters. Orally treated mangiferin at an effective dosage of 50 mg/kg bw, to DMBA painted hamsters were significantly averted the body weight, succession of tumour, the biochemical as well as histopathological changes. Conclusion Findings of this work clearly suggest that the anti‐carcinoma effect of mangiferin possesses the modulator effects on potent antioxidant, anti‐LPO and detoxification agents to expel the metabolites of malignant cells, on DMBA‐provoked BPC in hamsters.
This prospective, single-center study evaluated the clinical utility of annenxin (Anx)A1 level as a biomarker for determining the severity of illness and predicting the risk of death in hospitalized patients with community-acquired pneumonia (CAP). A total of 105 patients (53 with severe [S]CAP, 52 with non-SCAP) were enrolled from December 2020 to June 2021. Demographic and clinical data were recorded. Serum AnxA1 concentration on days one and six after admission was measured by enzyme-linked immunosorbent assay. AnxA1 level at admission was significantly higher in SCAP patients than in non-SCAP patients (p < 0.001) irrespective of CAP etiology and was positively correlated with Pneumonia Severity Index and Confusion, Uremia, Respiratory Rate, Blood Pressure, and Age ≥ 65 Years score. AnxA1 level was significantly lower on day six after treatment than on day one (p = 0.01). Disease severity was significantly higher in patents with AnxA1 level ≥254.13 ng/mL than in those with a level <254.13 ng/mL (p < 0.001). Kaplan–Meier analysis of 30-day mortality showed that AnxA1 level ≤670.84 ng/mL was associated with a significantly higher survival rate than a level >670.84 ng/mL. These results indicate that AnxA1 is a useful biomarker for early diagnosis and prognostic assessment of CAP.
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