Search Results (20)

Objectives: Contrast-induced acute kidney injury (CI-AKI) remains a frequent and serious complication after cardiac catheterization. Sirtuin-1 (SIRT1), a NAD+-dependent deacetylase, plays a central role in renal protection against ischemia-reperfusion injury, inflammation, and vascular dysfunction. We aimed to investigate whether serum SIRT1 levels could serve as an early diagnostic biomarker for CI-AKI. Methods: This prospective case-control study included 50 patients undergoing elective percutaneous coronary intervention (PCI) for stable angina. Serum SIRT1 levels were measured at baseline, 24 h, and 72 h post-PCI. The occurrence of CI-AKI was defined by a standard rise in serum creatinine, and patients were stratified accordingly. Results: Although SIRT1 levels tended to be lower in patients who developed CI-AKI (n = 17) compared to those without (n = 33), the differences were not statistically significant at any time point (p > 0.05). However, a significant between-group difference was observed in the 72-h change in SIRT1 levels (Δ0–72 h, p = 0.037), with a greater decline in the CI-AKI group. Multivariable logistic regression also revealed a trend-level inverse association between 72-h SIRT1 levels and CI-AKI (β = −0.536, p = 0.099). Conclusions: While SIRT1 is biologically plausible as a renal protective factor, our findings suggest that serial SIRT1 measurement may offer added value as a dynamic biomarker rather than a static diagnostic tool. Confirmatory trials incorporating serial SIRT1 measurements may help translate this molecular signal into clinically actionable tools for early detection of CI-AKI. Full article

Background: The inflammatory response is critically important in ST-segment elevation myocardial infarction (STEMI). The systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI), novel inflammatory biomarkers, have been linked to the determination of outcomes in various diseases. The aim of the current study was to examine the relation of the SII and SIRI with contrast-induced acute kidney injury (CI-AKI) in elderly subjects with STEMI undergoing primary percutaneous coronary intervention (pPCI). Methods: All patients diagnosed with STEMI between November 2020 and September 2024 were screened, and patients aged over 70 were retrospectively analyzed in the present study. The patients were divided into two groups according to CI-AKI development. The SII and SIRI were calculated based on the peripheral blood counts. A receiver operating characteristic (ROC) curve analysis was performed to determine the sensitivity and specificity of the SII and SIRI in predicting CI-AKI. Additionally, multivariable logistic regression models were employed to investigate the associations between inflammatory indices and the incidence of CI-AKI in elderly patients with STEMI. Results: A total of 263 participants were included (mean age 77.67 ± 6.20, 56% women). Both the SII and SIRI were higher in the CI-AKI group than in the non-CI-AKI group (3252 ± 2257, 1097 ± 991 p < 0.001 for SII; 12.1 ± 4.54, 4.86 ± 2.42 p < 0.006 for SIRI). In the receiver operating characteristic analysis, the SII and SIRI showed the highest area under curve (AUC) compared with other inflammatory parameters. The AUC of the SII and SIRI were 0.903 and 0.867 (p < 0.001). In multivariate logistic regression analysis, the SII and SIRI were found as independent predictors of CI-AKI. Conclusions: The SII and SIRI were found to be important markers for predicting post-procedural CI-AKI in elderly patients with STEMI. Full article

Contrast-induced acute kidney injury (CIAKI) is a common complication with limited treatments. Intermedin (IMD), a peptide belonging to the calcitonin gene-related peptide family, promotes vasodilation and endothelial stability, but its role in mitigating CIAKI remains unexplored. This study investigates the protective effects of IMD in CIAKI, focusing on its mechanisms, particularly the cAMP/Rac1 signaling pathway. Human umbilical vein endothelial cells (HUVECs) were treated with iohexol to simulate kidney injury in vitro. The protective effects of IMD were assessed using CCK8 assay, flow cytometry, ELISA, and Western blotting. A CIAKI rat model was utilized to evaluate renal peritubular capillary endothelial cell injury and renal function through histopathology, immunohistochemistry, immunofluorescence, Western blotting, and transmission electron microscopy. In vitro, IMD significantly enhanced HUVEC viability and mitigated iohexol-induced toxicity by preserving intercellular adhesion junctions and activating the cAMP/Rac1 pathway, with Rac1 inhibition attenuating these protective effects. In vivo, CIAKI caused severe damage to peritubular capillary endothelial cell junctions, impairing renal function. IMD treatment markedly improved renal function, an effect negated by Rac1 inhibition. IMD protects against renal injury in CIAKI by activating the cAMP/Rac1 pathway, preserving peritubular capillary endothelial integrity and alleviating acute renal injury from contrast media. These findings suggest that IMD has therapeutic potential in CIAKI and highlight the cAMP/Rac1 pathway as a promising target for preventing contrast-induced acute kidney injury in at-risk patients, ultimately improving clinical outcomes. Full article

The utilization of contrast media (CM) in clinical diagnostic imaging and interventional procedures has escalated, leading to a gradual increase in the incidence of contrast-induced acute kidney injury (CI-AKI). Presently, the scarcity of effective pharmacological treatments for CI-AKI poses significant challenges to clinical management. Firstly, we explore the pathogenesis of CI-AKI in this review. Beyond renal medullary ischemia and hypoxia, oxidative stress, cellular apoptosis, and inflammation, emerging mechanisms such as ferroptosis, release of neutrophil extracellular traps (NETs), and nitrosative stress, which offer promising avenues for the management of CI-AKI, are identified. Secondly, a comprehensive strategy for the early prevention of CI-AKI is introduced. Investigating the risk factors associated with CI-AKI is essential for the timely identification of high-risk groups. Additionally, exploring early sensitive biomarkers is crucial for early diagnosis. A synergistic approach that combines these sensitive biomarkers, CI-AKI risk factors, and disease risk prediction models enhances both the accuracy and efficiency of early diagnostic processes. Finally, we explore recent pharmacological and non-pharmacological interventions for the management of Cl-AKI. Beyond the traditional focus on the antioxidant N-acetylcysteine (NAC), we look at active compounds from traditional Chinese medicine, including tetramethylpyrazine (TMP), salvianolic acid B (Sal B), as well as emerging preventive medications like N-acetylcysteine amide (NACA), alprostadil, and others, which all showed potential benefits in animal and clinical studies for CI-AKI prevention. Furthermore, innovative strategies such as calorie restriction (CR), enhanced external counterpulsation (EECP), and mesenchymal stem cell therapy are highlighted as providing fresh insights into Cl-AKI prevention and management. Full article

(1) Background: This single-center retrospective study aimed to evaluate whether sodium–glucose cotransporter-2 inhibitors (SGLT2-i) therapy may have a nephroprotective effect to prevent contrast-induced acute kidney injury (CI-AKI) in patients with heart failure (HF) undergoing iodinated contrast medium (ICM) invasive procedures. (2) Methods: The population was stratified into SGLT2-i users and SGLT2-i non-users according to the chronic treatment with gliflozins. The primary endpoint was CI-AKI incidence during hospitalization. Secondary endpoints were all-cause mortality and the need for continuous renal replacement therapy (CRRT). (3) Results: In total, 86 patients on SGLT2-i and 179 patients not on SGLT2-i were enrolled. The incidence of CI-AKI in the gliflozin group was lower than in the non-user group (9.3 vs. 27.3%, p < 0.001), and these results were confirmed after propensity matching analysis. Multivariable logistic regression showed that only SGLT2-i treatment was an independent preventive factor for CI-AKI (OR: 0.41, 95% CI: 0.16–0.90, p = 0.045). The need for CRRT was reported only in five patients in the non-SGLT2-i-user group compared to zero patients in the gliflozin group (p = 0.05). (4) Conclusions: SGLT2-i therapy was associated with a lower risk of CI-AKI in patients with HF undergoing ICM invasive procedures. Full article

Contrast-Induced Acute Kidney Injury (CI-AKI) remains a frequent iatrogenic condition since radiological procedures using intra-vascular iodinated contrast media (CM) are being widely administered for diagnostic and therapeutic purposes. Despite the improvement of the medical healthcare system worldwide, CI-AKI is still associated with direct short-term and indirect long-term outcomes including increased morbidity and mortality, especially in patients with underlying pre-existing renal function impairment, cardiovascular disease, or diabetes that could rapidly progress into Chronic Kidney Disease. Although the RIFLE (Risk, Injury, Failure, Loss, End-Stage Kidney Disease), AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease Improving Global Outcomes) clinical criteria and recommendation guidelines are based on traditional “gold standard” biomarkers known as serum creatinine, glomerular filtration rate, and urinary output, new reliable serum and urinary biomarkers are still needed for an effective unified diagnostic strategy for AKI. Starting from previous and recent publications on the benefits and limitations of validated biomarkers responding to kidney injury, glomerular filtration, and inflammation among others, this review unravels the role of new emerging biomarkers used alone or in combination as reliable tools for early diagnosis and prognosis of CI-AKI, taking into account patients and procedures-risk factors towards a new clinical perspective. Full article

Background: Traditionally, mechanical thrombectomy performed for pulmonary embolism (PE) necessitates the utilization of iodinated contrast. Intravascular ultrasound (IVUS) has been used as a diagnostic and therapeutic modality in the management of acute high and intermediate-risk PE. Recently, with the shortage of contrast supplies and the considerable incidence of contrast-induced acute kidney injury (CI-AKI), other safer and more feasible IVUS methods have become desirable. The purpose of this systematic review was to evaluate the importance of IVUS in patients with PE undergoing thrombectomy. Methods: Medline/PubMed, Embase, Scopus, and Google Scholar were searched for review studies, case reports, and case series. Clinical characteristics, outcomes and the usage of IVUS-guided mechanical thrombectomy during the treatment of acute high and intermediate-risk PE were examined in a descriptive analysis. Results: In this systematic review, we included one prospective study, two case series, and two case reports from July 2019 to May 2023. A total of 39 patients were evaluated; most were female (53.8%). The main presenting symptoms were dyspnea and chest pain (79.5%); three patients (7.9%) presented with syncope, one with shock and one with cardiac arrest. Biomarkers (troponin and BNP) were elevated in 94.6% of patients. Most patients (87.2%) had intermediate-risk PE, and 12.8% had high-risk PE. All patients presented with right-heart strain (RV/LV ratio ≥ 0.9, n = 39). Most patients (56.4%) had bilateral PE. Mechanical thrombectomy was performed using IVUS without contrast utilization in 39.4% of the patients. After the initial learning curve, contrast usage decreased gradually over time. There was a significant decrease in the composite mean arterial pressure immediately following IVUS-guided thrombectomy from 35.1 ± 7.2 to 25.2 ± 8.3 mmHg (p < 0.001). Post-procedure, there was no reported (0%) CI-AKI, no all-cause mortality, no major bleeding, or other adverse events. There was a significant improvement in symptoms and RV function at the mean follow-up. Conclusions: New evidence suggests that IVUS-guided mechanical thrombectomy is safe, with visualization of the thrombus for optimal intervention, and reduces contrast exposure. Full article

Contrast-induced acute kidney injury (CI−AKI) is manifested by an abrupt decline in kidney function as a consequence of intravascular exposure to contrast media. With the increased applicability of medical imaging and interventional procedures that utilize contrast media for clinical diagnosis, CI−AKI is becoming the leading cause of renal dysfunction. The pathophysiological mechanism associated with CI−AKI involves renal medullary hypoxia, the direct toxicity of contrast agents, oxidative stress, apoptosis, inflammation, and epigenetic regulation. To date, there is no effective therapy for CI−AKI, except for the development of strategies that could reduce the toxicity profiles of contrast media. While most of these strategies have failed, evidence has shown that the proper use of personalized hydration, contrast medium, and high-dose statins may reduce the occurrence of CI−AKI. However, adequate risk predication and attempts to develop preventive strategies can be considered as the key determinants that can help eliminate CI−AKI. Additionally, a deeper understanding of the pathophysiological mechanism of CI−AKI is crucial to uncover molecular targets for the prevention of CI−AKI. This review has taken a step further to solidify the current known molecular mechanisms of CI−AKI and elaborate the biomarkers that are used to detect early-stage CI−AKI. On this foundation, this review will analyze the molecular targets relating to apoptosis, inflammation, oxidative stress, and epigenetics, and, thus, provide a strong rationale for therapeutic intervention in the prevention of CI−AKI. Full article

Introduction: Contrast-induced acute kidney injury (CIAKI) is one of the main causes of acute renal failure in hospitalized patients, following the administration of iodinated contrast medium used for CT scans and angiographic procedures. CIAKI determines a high cardiovascular risk and appears to be one of the most feared complications of coronary angiography, causing a notable worsening of the prognosis with high morbidity and mortality. Aim: To evaluate a possible association between the renal resistive index (RRI) and the development of CIAKI, as well as an association with the main subclinical markers of atherosclerosis and the main cardiovascular risk factors. Materials and Methods: We enrolled 101 patients with an indication for coronary angiography. Patients underwent an assessment of renal function (serum nitrogen and basal creatinine, 48 and 72 h after administration of contrast medium), inflammation (C reactive protein (CRP), serum calcium and phosphorus, intact parathormone (iPTH), 25-hydroxyvitaminD (25-OH-VitD), serum uric acid (SUA), total cholesterol, serum triglycerides, serum glucose and insulin). All patients also carried out an evaluation of RRI, intima-media thickness (IMT), interventricular septum (IVS) and the ankle-brachial index (ABI). Results: 101 patients (68 male), with a mean age of 73.0 ± 15.0 years, were enrolled for the study; 35 are affected by type 2 diabetes mellitus. A total of 19 cases of CIAKI were reported (19%), while among diabetic patients we reported an incidence of 23% (8 patients). In our study, patients with CIAKI had significantly higher RRI (p < 0.001) and IMT (p < 0.001) with respect to the patients who did not develop CIAKI. Furthermore, patients with CIAKI had significantly higher CRP (p < 0.001) and SUA (p < 0.006). Conclusions: We showed a significant difference in RRI, IMT, SUA and CRP values between the population developing CIAKI and patients without CIAKI. This data appears relevant considering that RRI and IMT are low-cost, non-invasive and easily reproducible markers of endothelial dysfunction and atherosclerosis. Full article

Contrast-induced acute kidney injury (CI-AKI) is a serious complication after angiographic examinations in cardiology. Diagnosis may be delayed based on standard serum creatinine, and subclinical forms of kidney damage may not be detected at all. In our study, we investigate the clinical use in these directions of a “damage”-type biomarker—neutrophil gelatinase-associated lipocalin (NGAL). Among patients with a high-risk profile undergoing scheduled coronary angiography and/or angioplasty, plasma NGAL was determined at baseline and at 4th and 24th h after contrast administration. In the CI-AKI group, NGAL increased significantly at the 4th hour (Me 109.3 (IQR 92.1–148.7) ng/mL versus 97.6 (IQR 69.4–127.0) ng/mL, p = 0.006) and at the 24th hour (Me 131.0 (IQR 81.1–240.8) ng/mL, p = 0.008). In patients with subclinical CI-AKI, NGAL also increased significantly at the 4th hour (Me 94.0 (IQR 75.5–148.2) ng/mL, p = 0.002) and reached levels close to those in patients with CI-AKI. Unlike the new biomarker, however, serum creatinine did not change significantly in this group. The diagnostic power of NGAL is extremely good—AUC 0.847 (95% CI: 0.677–1.000; p = 0.001) in CI-AKI and AUC 0.731 (95% CI: 0.539–0.924; p = 0.024) in subclinical CI-AKI. NGAL may be a reliable biomarker for the early diagnosis of clinical and subclinical forms of renal injury after contrast angiographic studies. Full article

Contrast-induced acute kidney injury (CI-AKI) can lead to the development of chronic kidney disease (CKD) and impaired in-hospital and long-term outcomes among cardiac patients. The aim of this study was to evaluate the impact of repeated contrast media (CM) administration during a single hospitalization on the rate of CI-AKI. The study group (n = 138) comprised patients with different diagnoses who received CM more than once during hospitalization, while the control group (n = 153) involved CAD patients subject to a single CM dose. Following propensity score matching (PSM), both groups of n = 84 were evenly matched in terms of major baseline variables. CI-AKI was defined by an absolute increase in SCr ≥ 0.3 mg/dL or >50% relative to the baseline value within 48–72 h from the last CM dose. Patients in the study group were older, had a higher prevalence of diabetes and CKD, received a higher total volume of CM, had a lower left ventricular ejection fraction, lower prevalence of multivessel coronary artery disease (MV-CAD), and a trend towards a lower prevalence of arterial hypertension and smoking. SCr did not differ between the study and control groups at 72 h after the CM use. CI-AKI occurred in 18 patients in the study (13.0%) and in 18 patients (11.8%) in the control group (p = 0.741). The rate of CI-AKI was also comparable following the PSM (13.1% vs. 13.1%, p = 1.0). Logistic regression analysis revealed that CKD, diabetes mellitus, MV-CAD, age, and non-steroidal anti-inflammatory drugs use, but not repeated CM use, were independent predictors of CI-AKI. Full article

Multivessel coronary artery disease (MVCAD) is found in approximately 50% of patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Although we have data showing the benefits of revascularization of significant non-culprit coronary lesions in patients with AMI, the optimal timing of angioplasty remains unclear. The most common reason for postponing subsequent percutaneous treatment is the fear of contrast-induced acute kidney injury (CI-AKI). Acute kidney injury (AKI) is common in patients with AMI undergoing PCI, and its etiology appears to be complex and incompletely understood. In this review, we discuss the definition, pathophysiology and risk factors of AKI in patients with AMI undergoing PCI. We present the impact of AKI on the course of hospitalization and distant prognosis of patients with AMI. Special attention was paid to the phenomenon of AKI in patients undergoing multivessel revascularization. We analyze the correlation between increased exposure to contrast medium (CM) and the risk of AKI in patients with AMI to provide information useful in the decision-making process about the optimal timing of revascularization of non-culprit lesions. In addition, we present diagnostic tools in the form of new biomarkers of AKI and discuss ways to prevent and mitigate the course of AKI. Full article

Neutrophil gelatinase-associated lipocalin (NGAL) has been proposed as an early marker for estimating the risk of contrast-induced acute kidney injury (CI-AKI). However, the predictive value of baseline serum NGAL levels for CI-AKI remains unclear. Serum NGAL was measured before percutaneous coronary intervention in 633 patients with coronary artery disease. The primary clinical endpoints were a composite of major adverse cardiac and cerebrovascular events (MACCEs; cardiac death, myocardial infarction, stroke, and any revascularization). The mean follow-up duration was 29.4 months. Ninety-eight (15.5%) patients developed CI-AKI. Compared with patients without CI-AKI, baseline serum NGAL was higher in patients with CI-AKI (149.6 ± 88.8 ng/mL vs. 138.0 ± 98.6 ng/mL, p = 0.0279), although serum creatinine and estimated glomerular filtration rate were not different between groups. Patients in the highest tertile of baseline serum NGAL showed a significantly higher rate of MACCEs (10.5% vs. 3.8%, p = 0.02). Using the first tertile as a reference, the adjusted hazard ratios for MACCEs in patients in the second and third tertiles of NGAL were 2.151 (confidence interval (CI) 0.82 to 5.59, p = 0.116) and 2.725 (CI 1.05 to 7.05, p = 0.039), respectively. Baseline serum NGAL is a reliable marker for predicting CI-AKI, and high serum NGAL levels are associated with a higher incidence rate of long term MACCEs. Full article

Background: The risk of contrast-induced acute kidney injury (CI-AKI) following coronary intervention is particularly high among patients with chronic kidney disease (CKD). Among these patients, baseline neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubular damage, reflects the severity of renal impairment. We evaluated whether the baseline serum NGAL level may be a marker for the development of CI-AKI following percutaneous coronary intervention (PCI). Methods: Eighty-eight CKD patients treated with PCI were included. Serum NGAL levels were drawn upon hospital admission. Receiver operator characteristic (ROC) methods were used to identify the optimal sensitivity and specificity for the observed NGAL level compared with the estimated glomerular filtration rate (eGFR) calculated for patients with CI-AKI. Results: Overall CI-AKI incidence was 43%. Baseline serum NGAL levels were significantly higher in patients with CI-AKI than in patients without CI-AKI (150 vs. 103 ng/mL, p < 0.001). According to the ROC curve, baseline NGAL levels performed better than eGFR to predict CI-AKI (AUC 0.753 vs. 0.604), with the optimal cutoff value for baseline NGAL to predict CI-AKI being 127 ng/mL (sensitivity of 68% and specificity of 68%, p < 0.001). In a multivariate logistic regression model, the NGAL level >127 ng/mL ng/mL was independently associated with CI-AKI (HR 9.84, 95% CI: 1.96–40.3; p = 0.01). Conclusion: Baseline serum NGAL levels in CKD patients may identify a high-risk population for CI-AKI following PCI. Further studies on larger populations are required to validate the potential utility of NGAL measurements in monitoring specific CKD-associated conditions. Full article

Endothelial dysfunction plays key roles in the pathological process of contrast media (CM)-induced acute kidney injury (CI-AKI) in patients undergoing vascular angiography or intervention treatment. Previously, we have demonstrated that an apolipoprotein A-I (apoA-I) mimetic peptide, D-4F, inhibits oxidative stress and improves endothelial dysfunction caused by CM through the AMPK/PKC pathway. However, it is unclear whether CM induce metabolic impairments in endothelial cells and whether D-4F ameliorates these metabolic impairments. In this work, we evaluated vitalities of human umbilical vein endothelial cells (HUVECs) treated with iodixanol and D-4F and performed nuclear magnetic resonance (NMR)-based metabolomic analysis to assess iodixanol-induced metabolic impairments in HUVECs, and to address the metabolic mechanisms underlying the protective effects of D-4F for ameliorating these metabolic impairments. Our results showed that iodixanol treatment distinctly impaired the vitality of HUVECs, and greatly disordered the metabolic pathways related to energy production and oxidative stress. Iodixanol activated glucose metabolism and the TCA cycle but inhibited choline metabolism and glutathione metabolism. Significantly, D-4F pretreatment could improve the iodixanol-impaired vitality of HUVECs and ameliorate the iodixanol-induced impairments in several metabolic pathways including glycolysis, TCA cycle and choline metabolism in HUVECs. Moreover, D-4F upregulated the glutathione level and hence enhanced antioxidative capacity and increased the levels of tyrosine and nicotinamide adenine dinucleotide in HUVECs. These results provided the mechanistic understanding of CM-induced endothelial impairments and the protective effects of D-4F for improving endothelial cell dysfunction. This work is beneficial to further exploring D-4F as a potential pharmacological agent for preventing CM-induced endothelial impairment and acute kidney injury. Full article