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Contrast-induced acute kidney injury (CI-AKI) is an important complication following the use of iodinated contrast media. Bilirubin has a protective effect but may also aggravate CI-AKI. The purpose of this systematic review was to assess whether bilirubin is a risk factor for CI-AKI. We searched the databases PubMed, Embase, Web of Science, Cochrane Library, Scopus, Ovid Medline, CNKI (China National Knowledge Infrastructure), VPCS (Vip Paper Check System), Wanfang, and CBM (Chinese BioMedical Literature Database) from the initial date to May 6, 2023. We summarized the results by directly combining the effect-size odds ratio (OR) and 95% confidence interval (CI) and identified sources of heterogeneity through subgroup analysis, sensitivity analysis, and meta-regression analysis. A total of 10 studies (14 data sets) were included: 7 retrospective studies (10 data sets) and 3 prospective studies (4 data sets), involving 12776 participants. The incidence of CI-AKI of 16% (95% CI: 14-19%). Total bilirubin was positively associated with the occurrence of CI-AKI (OR = 1.80; 95% CI: 1.36-2.38). Both low and high bilirubin concentrations were risk factors for CI-AKI. The incidence of CI-AKI was higher in the low bilirubin group than in the high bilirubin group. [ABSTRACT FROM AUTHOR]

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies (P = .001, I2 = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: −0.52 mg/dL; 95% CI: −0.81 to −0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria. [ABSTRACT FROM AUTHOR]

Background Multi-modal CT ( MMCT) to guide decision making for reperfusion treatment is increasingly used, but there remains a perceived risk of contrast-induced nephropathy ( CIN). At our center, MMCT is used empirically without waiting for serum-creatinine ( sCR) or renal profiling. Aims To determine the incidence of CIN, examine the risk factors predisposing to its development, and investigate its effects on clinical outcome in the acute stroke population. Methods An institution-wide protocol was implemented for acute stroke presentations to have MMCT (100-150 ml nonionic tri-iodinated contrast, perfusion CT and CT angiography) without waiting for serum-creatinine to minimize delays. Intravenous saline is routinely infused (80-125 ml/h) for at least 24-h after MMCT. Serial creatinine levels were measured at baseline, risk period, and follow-up. Renal profiles and clinical progress were reviewed up to 90 days. Results We analyzed 735 consecutive patients who had MMCT for the evaluation of acute ischemic or hemorrhagic stroke during the last five-years. A total of 623 patients met the inclusion criteria for analysis: 16 cases (2·6%) biochemically qualified as CIN; however, the risk period serum-creatinine for 15 of these cases was confounded by dehydration, urinary tract infection, or medications. None of the group had progression to chronic kidney disease or required dialysis. Conclusions The incidence of CIN is low when MMCT is used routinely to assess acute stroke patients. In this population, CIN was a biochemical phenomenon that did not have clinical manifestations, cause chronic kidney disease, require dialysis, or negatively impact on 90-day mRS outcomes. Renal profiling and waiting for a baseline serum-creatinine are an unnecessary delay to emergency reperfusion treatment. [ABSTRACT FROM AUTHOR]

Currently, the number of imaging and interventional procedures that use contrast agents (CAs) is gradually increasing. Contrast-induced nephropathy (CIN) is the most important CA-related complication. Oxidative stress plays a significant role in its pathophysiology. Lycopene (LPN) is a natural substance with strong antioxidant capacity. The present study aimed to investigate the potential preventive effects of LPN against CIN. In total, 28 male Wistar albino rats were divided into 4 groups with 7 rats in each group; the groups include normal control group, LPN only group at a dose of 4 mg/kg/day for 10 days, CIN group by administering 10 mg/kg furosemide IM + 10 mg/kg indomethacin IP + 10 ml/kg iomeprol IV following 24-h dehydration, and CIN + LPN group. There were statistically significant increase in urea, creatinine, and malondialdehyde levels (p < 0.001, for all) but a significant decrease in glutathione, superoxide dismutase, catalase, and glutathione peroxidase levels (p < 0.001, for all) in the CIN group compared with the control group. On histological examination, a significant increase of infiltrated inflammatory cells and necrotic degenerative changes were observed in the CIN group and the immunohistochemical examination revealed a significant increase in inflammation (inducible nitric oxide synthase), autophagy (LC3/B), and apoptosis (cleaved caspase 3) in the CIN group compared with the control group (p < 0.05, for all). Significant improvements in these unfavorable parameters were observed with CIN + LPN group compared with the CIN only group. In conclusion, the favorable effects of LPN as an anti-inflammatory, antiautophagic, and antiapoptotic agent in an experimental model of CIN have been demonstrated. [ABSTRACT FROM PUBLISHER]

Contrast-induced nephropathy (CIN) refers to a decline in renal function following exposure to iodinated contrast media (CM). The present study was initiated to explore the role of known human risk factors (spontaneous hypertension, diabetes, protein-losing nephropathy) on CIN development in rodent models and to determine the effect of CM administration on kidney injury biomarkers in the face of preexisting kidney injury. Spontaneously hypertensive rats (hypertension), streptozotocin-treated Sprague Dawley rats (diabetes), and Dahl salt-sensitive rats (protein-losing nephropathy) were given single intravenous injections of the nonionic, low osmolar contrast medium, iohexol. Blood urea nitrogen (BUN), serum creatinine (sCr), and urinary biomarkers; albumin, lipocalin 2 (Lcn-2), osteopontin (Opn), kidney injury molecule 1 (Kim-1), renal papillary antigen 1 (Rpa-1), α-glutathione S-transferase (α-Gst), µ-glutathione S-transferase (µ-Gst), and beta-2 microglobulin (β2m) were measured in disease models and appropriate controls to determine the response of these biomarkers to CM administration. Each disease model produced elevated biomarkers of kidney injury without CM. Preexisting histopathology was exacerbated by CM but little or no significant increases in biomarkers were observed. When 1.5-fold or greater sCr increases from pre-CM were used to define true positives, receiver–operating characteristic curve analysis of biomarker performance showed sCr was the best predictor of CIN across disease models. β2m, Lcn-2, and BUN were the best predictors of histopathology defined kidney injury. [ABSTRACT FROM AUTHOR]

Peripheral arterial disease (PAD) is a common manifestation of atherosclerotic vascular disease and the incidence of infrapopliteal PAD continues to rise in the population. The historical experience with surgical and endovascular interventions for infrapopliteal stenosis was disappointing as operators experienced high rates of early technical failures and procedural complications, coupled with high rates of restenosis in this vascular territory when compared with more proximal vascular beds. While patients with infrapopliteal PAD may be asymptomatic, the majority would ultimately develop intermittent claudication or may also present with critical limb ischemia. In this article, we review the current literature, and discuss some of the technical aspects of endovascular therapy in this vascular bed. We also emphasize the importance of adjunctive evidence-based therapies such as antiplatelet agents, statins, and lifestyle modification such as smoking cessation in this particularly high-risk cohort to optimize clinical outcomes. [ABSTRACT FROM PUBLISHER]

Background: Previous studies that have attempted to evaluate the effectiveness of an iso-osmolar contrast medium (IOCM) iodixanol compared to a low-osmolar contrast medium (LOCM) for contrast procedures show variable results. Purpose: To evaluate the nephrotoxicity of the IOCM iodixanol compared to the LOCM iohexol. Material and Methods: We performed a retrospective cohort study from April 2004 to March 2006. All contrast procedures with a pre- and post-exposure creatinine value were evaluated for inclusion. Contrast nephropathy (CN) was defined as post-exposure creatinine elevation of ≥25% or >0.5 mg/dl within 7 days of contrast exposure. Cases of iodixanol exposure were matched to control cases of iohexol exposure (1:1) based on age, sex, presence of diabetes, pre-exposure creatinine value, and type of imaging study performed. We matched 397 cases of iodixanol (IOCM) exposure to 397 cases of iohexol (LOCM) exposure. Cases of iodixanol which could not be matched to controls were not included in the analysis. Results: After adjustment for prior creatinine, medications, contrast iodine load, prior exposure to contrast material, heart failure, and hypertension, use of iodixanol did not significantly alter rates of CN compared to iohexol (OR 0.92, 95% CI 0.57-1.46; P=0.71) or mortality (RR 0.79, 95% CI 0.59-1.06; P=0.12). Conclusion: The use of the IOCM iodixanol was not associated with statistically significant protection against contrast nephropathy or all-cause mortality compared to a matched cohort of patients receiving the LOCM iohexol. [ABSTRACT FROM AUTHOR]