Search Results (60)

Background/Objectives: Contrast agents can damage renal tissue through multiple mechanisms, particularly by increasing reactive oxygen species (ROS), which contribute to DNA oxidation, lipid peroxidation, and endothelial injury. This prospective, comparative study aimed to evaluate the changes in ROS-related gene expressions—NFKB1, SIRT1, NFE2L2, and FOXO1—in patients who developed contrast-induced nephropathy (CIN) following coronary angiography versus those who did not. Methods: A total of 48 patients undergoing primary percutaneous coronary intervention were enrolled. Twenty-three patients who developed CIN (Group 1) were compared to 25 matched controls without CIN (Group 2) based on age, gender, and comorbidities. Blood and serum samples were collected 72 h post-contrast exposure to assess biochemical markers and mRNA expression levels of the target genes. Results: The mean age was similar between the groups (63 ± 7 vs. 62 ± 6 years; p > 0.05), as was gender distribution. Group 1 showed significant increases in serum creatinine and reductions in e-GFR post-procedure. Importantly, NFKB1, NFE2L2, and FOXO1 mRNA expression levels were significantly upregulated in CIN patients—by 5.7-, 5.8-, and 4.97-fold, respectively, while SIRT1 expression was downregulated by 0.76-fold (p < 0.05). Conclusions: These findings indicate enhanced activation of inflammatory and oxidative stress pathways in CIN patients, particularly through the NF-κB signaling axis. Conversely, reduced SIRT1 expression suggests diminished antioxidant protection. The study highlights that ROS-related gene expression changes may serve as potential biomarkers for CIN progression. Further studies at the protein level are needed to clarify cytokine roles in these pathways. Full article

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

Mitochondrial dysfunction is a pivotal driver in the pathogenesis of acute kidney injury (AKI), chronic kidney disease (CKD), and congenital anomalies of the kidney and urinary tract (CAKUT). The kidneys, second only to the heart in mitochondrial density, rely on oxidative phosphorylation to meet the high ATP demands of solute reabsorption and filtration. Disrupted mitochondrial dynamics, such as excessive fission mediated by Drp1, exacerbate tubular apoptosis and inflammation in AKI models like ischemia–reperfusion injury. In CKD, persistent mitochondrial dysfunction drives oxidative stress, fibrosis, and metabolic reprogramming, with epigenetic mechanisms (DNA methylation, histone modifications, non-coding RNAs) regulating genes critical for mitochondrial homeostasis, such as PMPCB and TFAM. Epigenetic dysregulation also impacts mitochondrial–ER crosstalk, influencing calcium signaling and autophagy in renal pathology. Mitophagy, the selective clearance of damaged mitochondria, plays a dual role in kidney disease. While PINK1/Parkin-mediated mitophagy protects against cisplatin-induced AKI by preventing mitochondrial fragmentation and apoptosis, its dysregulation contributes to fibrosis and CKD progression. For instance, macrophage-specific loss of mitophagy regulators like MFN2 amplifies ROS production and fibrotic responses. Conversely, BNIP3/NIX-dependent mitophagy attenuates contrast-induced AKI by suppressing NLRP3 inflammasome activation. In diabetic nephropathy, impaired mitophagy correlates with declining eGFR and interstitial fibrosis, highlighting its diagnostic and therapeutic potential. Emerging therapeutic strategies target mitochondrial dysfunction through antioxidants (e.g., MitoQ, SS-31), mitophagy inducers (e.g., COPT nanoparticles), and mitochondrial transplantation, which mitigates AKI by restoring bioenergetics and modulating inflammatory pathways. Nanotechnology-enhanced drug delivery systems, such as curcumin-loaded nanoparticles, improve renal targeting and reduce oxidative stress. Epigenetic interventions, including PPAR-α agonists and KLF4 modulators, show promise in reversing metabolic reprogramming and fibrosis. These advances underscore mitochondria as central hubs in renal pathophysiology. Tailored interventions—ranging from Drp1 inhibition to mitochondrial transplantation—hold transformative potential to mitigate kidney injury and improve clinical outcomes. Additionally, dietary interventions and novel regulators such as adenogens are emerging as promising strategies to modulate mitochondrial function and attenuate kidney disease progression. Future research should address the gaps in understanding the role of mitophagy in CAKUT and optimize targeted delivery systems for precision therapies. Full article

Background/Objectives: Contrast-induced nephropathy (CIN) is a well-documented complication following coronary angiography and percutaneous coronary intervention (PCI). This study aims to evaluate the predictors of CIN and its effect on outcomes in patients with acute coronary syndrome (ACS). Methods: A retrospective study included 1579 patients who underwent coronary angiography or PCI. Results: The overall incidence of in-hospital CIN was 6.8%, with the highest incidence in the group with eGFR <30 mL/min/1.73 m² at 21.6%. Non-radial vascular access was an independent predictor of CIN occurrence (OR = 2.06 [1.37–3.08]; p < 0.001). The risk of death within 30 days was influenced by history of stroke (OR = 4.94 [1.58–15.51]; p = 0.006), glucose level on admission (per 10-unit increase) (OR = 1.07 [1.04–1.1]; p < 0.001), occurrence of CIN (OR = 5.64 [2.49–12.79]; p < 0.001), and hemoglobin level (OR = 0.77 [0.65–0.92]; p = 0.003). The risk of death within 365 days was increased by age (OR = 1.05 [1.02–1.07]; p < 0.001), history of stroke (OR = 2.45 [1.02–5.89]; p = 0.046), glucose levels on admission (per 10-unit increase) (OR = 1.05 [1.03–1.08]; p < 0.001), occurrence of CIN (OR = 2.62 [1.42–4.84]; p = 0.002), and hemoglobin concentration (OR = 0.78 [0.7–0.88]; p = 0.003). An independent predictor of hospitalization for acute or exacerbation of chronic renal failure was baseline creatinine concentration (OR = 3.44 [2.4–4.93]; p < 0.001). Conclusions: The incidence of CIN is significant, particularly in patients with severe pre-existing renal impairment. Non-radial vascular access is an independent predictor of CIN. The occurrence of CIN is a strong independent predictor of both short-term and long-term mortality. Full article

The phenomenon of contrast-induced nephropathy (CIN) and contrast-associated nephropathy (CAN) has been acknowledged for an extensive duration. Recently, there has been a significant rise in research on the topic due to the enhanced availability of imaging investigations. This theory has been thoroughly validated and extensively reported in the scholarly literature. The primary risk factors are chronic kidney disease, diabetes, sepsis, critical illness, circulatory shock, anemia, advanced age, inadequate hydration, and the use of nephrotoxic medications. The principal preventive strategies are the use of iso-osmolar contrast agents and sufficient hydration, which includes the use of intravenous isotonic saline. The administration of N-acetylcysteine has been shown to decrease the occurrence of CIN without impacting outcomes like mortality or the need for dialysis. Recently, a growing number of scholarly studies have contested this phenomenon, or at least, questioned its clinical significance, rendering it primarily a biochemical occurrence. This review aims to evaluate the previously listed studies. Overestimating the possible dangers of post-contrast nephropathy may diminish the sensitivity of imaging tests that may otherwise utilize contrast, so substantially lowering their clinical relevance. This hypothesis is critically significant to science, medicine, and patients, warranting attention despite the necessity for additional research to validate it. The present study demonstrates that the frequency and importance of CIN may be overestimated. Full article

Contrast-induced nephropathy (CIN) represents a significant complication associated with the use of iodinated contrast media (ICM), especially in individuals with preexisting renal impairment. The pathophysiology of CIN encompasses oxidative stress, inflammation, endothelial dysfunction, and hemodynamic disturbances, resulting in acute kidney injury (AKI). Early detection is essential for effective management; however, conventional markers like serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) exhibit limitations in sensitivity and timeliness. This review emphasizes the increasing significance of novel biomarkers in enhancing early detection and risk stratification of contrast-induced nephropathy (CIN). Recent advancements in artificial intelligence and computational analytics have improved the predictive capabilities of these biomarkers, enabling personalized risk assessment and precision medicine strategies. Additionally, we discuss mitigation strategies, including hydration protocols, pharmacological interventions, and procedural modifications, aimed at reducing CIN incidence. Incorporating biomarker-driven assessments into clinical decision-making can enhance patient management and outcomes. Future research must prioritize the standardization of biomarker assays, the validation of predictive models across diverse patient populations, and the exploration of novel therapeutic targets. Utilizing advancements in biomarkers and risk mitigation strategies allows clinicians to improve the safety of contrast-enhanced imaging and reduce the likelihood of renal injury. Full article

Introduction: Contrast-induced nephropathy (CIN) has emerged as a prevalent and serious complication associated with the administration of iodinated contrast media during diagnostic and therapeutic procedures. Given the rising global prevalence of chronic kidney disease(CKD,) it is crucial to gain a deeper understanding of the risks linked to contrast media exposure. Therefore, the aim of this study, conducted at the Vascular Surgery Clinic in a tertiary hospital in Eastern Europe (Timisoara, Romania), is to assess the incidence of CIN and identify its associated risk factors among patients undergoing endovascular interventions. Methods: This retrospective cohort study was conducted using data from patients treated at a vascular surgery clinic in Timisoara, Romania, between 1 January 2018 and 31 December 2023. The study population included adult patients who underwent scheduled endovascular procedures and had serum creatinine measurements both before and after the procedure. Results: A total of 331 patients were included in the analysis (71.42% males with a mean age of 66.79 ± 9.86 years). In total, 9.22% of the patients had CKD, while 23.8% developed CIN. The mean age was significantly higher in the CIN group (68.4 years) compared to the non-CIN group (66.32 years) with a p-value of 0.093, indicating that older age is associated with a higher risk of CIN. A multivariate logistic regression analysis was performed to assess the association between various factors and the development of CIN. Higher hemoglobin levels were associated with reduced odds of CIN (OR = 0.792, 95% CI: 0.659–0.952, p = 0.0148), indicating that anemia is a significant risk factor for CIN, while CKD significantly increased the odds of CIN by 85.8% (OR = 1.858, 95% CI: 1.105–3.125, p = 0.0023), establishing CKD as a critical risk factor for CIN. Conclusions: While anemia and CKD were found to be significant predictors of CIN, further research on a wider population is required to validate these findings and explore additional risk factors. Our study shows that, in the context of elective endovascular procedures, addressing anemia correction and stabilizing creatinine levels to baseline represents a crucial strategy for reducing the risk of CIN. Full article

Background: Hypertriglyceridemia has serious health risks such as cardiovascular disease, type 2 diabetes mellitus, nephropathy, and others. Fenofibrate is an effective hypolipidemic drug, but its benefits for ameliorating disorders associated with hypertriglyceridemia failed to be proven in clinical trials. Methods: To search for possible causes of this situation and possibilities of their favorable influence, we tested the effect of FF monotherapy and the combination of fenofibrate with silymarin on metabolic disorders in a unique model of hereditary hypertriglyceridemic rats (HHTg). Results: Fenofibrate treatment (100 mg/kg BW/day for four weeks) significantly decreased serum levels of triglyceride, (−77%) and free fatty acids (−29%), the hepatic accumulation of triglycerides, and the expression of genes encoding transcription factors involved in lipid metabolism (Srebf2, Nr1h4. Rxrα, and Slco1a1). In contrast, the hypertriglyceridemia-induced ectopic storage of lipids in muscles, the heart, and kidneys reduced glucose utilization in muscles and was not affected. In addition, fenofibrate reduced the activity of the antioxidant system, including Nrf2 expression (−35%) and increased lipoperoxidation in the liver and, to a lesser extent, in the kidneys and heart. Adding silymarin (micronized form, 600 mg/kg BW/day) to fenofibrate therapy increased the synthesis of glycogen in muscles, (+36%) and reduced hyperinsulinemia (−34%). In the liver, it increased the activity of the antioxidant system, including PON-1 activity and Nrf2 expression, and reduced the formation of lipoperoxides. The beneficial effect of combination therapy on the parameters of oxidative stress and lipoperoxidation was also observed, to a lesser extent, in the heart and kidneys. Conclusions: Our results suggest the potential beneficial use of the combination of FF with SLM in the treatment of hypertriglyceridemia-induced metabolic disorders. Full article

Background: Having a laboratory renal profile for medical imaging examinations requiring contrast media (CM) administration is strongly advised. Creatinine helps identify patients at risk of contrast-induced nephropathy (CIN). The GEM^® Premier™ ChemSTAT (Werfen) is a point-of-care (POC) analyzer with 12 emergency parameters, including a creatinine assay. This study aims to compare ChemSTAT with the central analytical solution of the University Hospital of Clermont-Ferrand and to evaluate the interest in using POC creatinine in the emergency department (ED) to optimize the flow of patients, especially when CM administration is necessary. Methods: More than 200 whole blood (WB) samples from the ED were evaluated on the ChemSTAT analyzer. As comparative methods, the plasma aliquots from the same samples were assayed on an Atellica^® CH (Siemens Healthineers). The clinical concordance was assessed according to the decision cut-offs of the French Society of Radiology for the risk of CIN. The availability times of biological results between ChemSTAT and the central laboratory were studied. Results: WB results from the ChemSTAT analyzer correlated well with those from the Atellica^® CH, except for tCO2 (the known bias between the Siemens and Cobas Roche methods for predicting ChemSTAT values). The results of the creatinine assay allow for identical medical decisions in comparison to the renal-risk cut-offs. The availability of the biological results was reduced by 50 min on average with ChemSTAT vs the central laboratory. Computed tomography (CT) was performed for 44.7% of patients, including the injection of the CM in 68% of cases. For these patients, the availability of creatinine results relative to imaging time is faster with the ChemSTAT by an average of 45.2 min. Conclusions: Great analytical and clinical correlations for creatinine assays allow for the safe identification of patients at risk of CIN, and improve patient flow in ED, especially for those requiring computed tomography with CM. Full article

Background: Our study aims to provide an overview of existing evidence regarding the image quality of dual-energy CT (DECT) employing reduced contrast media (CM) volumes, in comparison to single-energy CT (SECT) with standard CM loads. The advantages, indications, and possible applications of DECT were investigated from the perspective of providing better patient care, minimizing CM volume and managing CM shortage. Methods: In this systematic review (PRISMA methodology), PubMed and WOS were searched from January 2010 to January 2023 by two independent reviewers. The scan and CM characteristics, radiation dose, and results of quantitative (contrast to noise ratio, CNR, and signal to noise ratio, SNR) and qualitative assessment of image quality were collected. Sixty non-duplicated records eligible for full-text screening were examined. Results: Finally, 22 articles (1818 patients) were included. The average CM reduction with DECT ranged between 43.4 ± 11%. Despite the wide variability in CT scan protocols, no differences were found in radiation doses between DECT and SECT. Conclusions: DECT scanners allow the employment of lower CM volumes with equal or better image quality evaluated by quantitative and qualitative analyses and similar dose radiation compared to SECT. Using image reconstructions at low monochromatic energy levels, DECT increases iodine conspicuity and attenuation contributing to CM containment measures. 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

Acute kidney injury following trauma impacts patient recovery critically, necessitating an integrated approach to emergency care and nephrology. This review aims to provide a comprehensive understanding of trauma-induced nephropathy, highlighting recent advancements in pathophysiological insights, diagnostic techniques, and strategic interventions. Our key findings emphasize the role of biomarkers, like Neutrophil Gelatinase-Associated Lipocalin and Liver Fatty Acid-Binding Protein, and imaging techniques, such as contrast-enhanced ultrasound, in early AKI detection. Preventive strategies, including aggressive fluid resuscitation, avoidance of nephrotoxic agents, and hemodynamic optimization, are essential for mitigating AKI progression. Integrating these approaches into trauma care frameworks aims to enhance patient outcomes and set a foundation for future research and clinical improvements. Full article

Purpose: To compare the efficacy and safety of percutaneous mechanical debulking (PMD) using mechanical rotational atherectomy combined with paclitaxel drug-coated balloon (DCB) versus using paclitaxel DCB alone in the treatment of in-stent restenosis. Material and Methods: This is a multicentric retrospective observational study conducted over a period of 2 years from 2020 to 2022. The study included 49 patients presented with chronic limb-threatening ischemia (CLTI) associated with in-stent restenosis, either acute (<14 days), subacute (<3 months) or chronic (>3 months). The enrolled patients underwent endovascular revascularization using either PMD combined with paclitaxel DCB or paclitaxel DCB only. They were followed up for 6 months after the intervention clinically and by duplex evaluation. Results: The lesion length was about 14.2 mm in the group treated by PMD+ DCB and 9.3 mm in the group treated by DCB alone. The technical success rate was the same between the two groups. However, the follow-up after 6 months showed that patencies for PMD + DCB and DCB alone were 15 (68.2%) patients and 15 (55.6%) patients, respectively (significant p value = 0.028). Procedural-related complications for PMD + DCB are distal embolization (9%) of cases and no vessel perforation. Regarding the candidates who were treated by DCB alone, there were minor groin hematomas (11.1%), distal arterial thrombosis (11.1%) and contrast-induced nephropathy (CIN) (11.1%) cases. Conclusion: The endovascular management of in-stent restenosis using percutaneous mechanical debulking (PMD) in conjunction with paclitaxel drug-coated balloon (DCB) showed that PMD combined with DCB is a safe and effective modality for achieving recanalization. It gives a satisfactory outcome in terms of technical success, freedom from clinically driven target lesion revascularization rate (CD-TLR) and mortality. Despite these promising results, further research with a large enrolled population may be required to determine the cost/benefit. Full article

Background. Lower extremity peripheral artery disease (LEPAD) frequently coexists with coronary artery disease (CAD) in patients with multisite vascular disease (MVD). While percutaneous revascularization is well-established for both LEPAD and CAD, limited evidence exists for patients eligible for both procedures. Specifically, the feasibility of concomitant LEPAD and CAD percutaneous revascularization remains unknown. Objectives. To compare the efficacy and safety of concomitant coronary and lower extremity elective percutaneous revascularization. Methods. Between 2012 and 2021, we included 135 patients in an observational, retrospective single-center registry. The population was stratified into two groups: 45 patients (concomitant group) underwent simultaneous coronary and peripheral percutaneous interventions, and 90 patients (deferred group) underwent two separate procedures within one year. The primary efficacy endpoint was major adverse cardiovascular events (MACE) at one year, while the primary safety endpoint was in-hospital contrast-induced nephropathy (CIN). Results. Study groups were well-balanced in baseline characteristics. In terms of coronary features, the concomitant revascularization group more often underwent single-vessel percutaneous coronary intervention (PCI), while the deferred group had multivessel PCI with diffuse coronary disease. No differences were detected in the number of LEPAD lesions between groups. For the primary efficacy endpoint, the incidence of MACE at one year was 37.8% in the concomitant group vs. 34.4% in the deferred group (HR 1.20, 95% CI 0.64–2.10; p = 0.61). No significant differences were found in CIN occurrence between the concomitant and deferred groups (11.1% vs. 8.9%; OR 1.30; 95% CI 0.36–4.21; p = 0.68). Conclusions. Multisite vascular disease patients eligible for CAD and LEPAD percutaneous revascularization exhibited a high cardiovascular risk profile with diffuse multivessel coronary and lower extremity disease. Our study suggests the efficacy and safety of concomitant coronary and lower extremity percutaneous revascularization based on one-year MACE incidence and in-hospital CIN. However, dedicated studies are warranted to confirm the short- and long-term outcomes of the concomitant revascularization strategy. Full article

Background: Contrast-induced nephropathy (CIN) is one of the most important complications after invasive cardiovascular procedures. Considering the pivotal role of inflammation in CIN development, the use of peripheral blood-based indexes may be an easily available biomarker to predict CIN risk. Therefore, in the present study, we evaluated the association between the pan-immune-inflammation value (PIV) and the risk of CIN. Patients and Methods: A total of 1343 patients undergoing coronary angiography (CAG) were included. The PIV was calculated with the following equation: (neutrophil count × platelet count × monocyte count)/lymphocyte count. Multivariable regression analyses were used to determine the association between clinical and laboratory parameters and CIN development. Results: The median age of the cohort was 58 (IQR 50–67), and 48.2% of the patients were female. CIN developed in 202 patients (15%) in follow-up. In multivariate analyses, older age (OR: 1.015, 95% CI: 1.002–1.028, p = 0.020) and higher PIV levels (OR: 1.016, 95% CI: 1.004–1.028, p = 0.008) were associated with a higher CIN risk, while the use of antiplatelet agents was associated with a lower risk of CIN (OR: 0.670, 95% CI: 0.475–0.945, p = 0.022). Conclusions: We demonstrated that the risk of CIN was significantly higher in patients with higher PIV and older patients in a large cohort of patients undergoing CAG for stable ischemic heart disease. If supported with prospective evidence, PIV levels could be used as a minimally invasive reflector of CIN. Full article