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Contrast-induced acute kidney injury (CI-AKI) is one of the main causes of hospital-acquired renal failure, and still lacks of effective treatments. Previously, we demonstrated that αKlotho, which is an anti-aging protein that highly expresses in the kidney, has therapeutic activity in CI-AKI through promoting autophagy. However, the specific mechanism underlying αKlotho-mediated autophagy remains unclear. The RNA sequencing analysis of renal cortex revealed that the differentially expressed genes related to autophagy between αKlotho-treated CI-AKI mice and vehicle-treated CI-AKI mice were found to be associated with mitophagy and apoptosis. In the kidney of CI-AKI mice and HK-2 cells exposed to Iohexol, we revealed that αKlotho promoted mitophagy and decreased cell apoptosis. Mechanistically, αKlotho attenuated mitochondria damage, decreased mitochondrial ROS by upregulating BNIP3-mediated mitophagy. BNIP3 deletion abolished the beneficial effects of αKlotho both in vivo and in vitro. Moreover, we further demonstrated that αKlotho upregulated FoxO3 nuclear expression in Iohexol-treated HK-2 cells. Knockdown of FOXO3 gene inhibited αKlotho-promoted BNIP3-mediated mitophagy and subsequently increased the oxidative injury and cell apoptosis. Taken together, our results indicated a critical role of αKlotho in alleviating CI-AKI via mitophagy promotion involving the FoxO3-BNIP3 pathway., Competing Interests: Declarations Ethical approval All animal experiments were approved by the Animal Care Committee at the Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, and performed according to the Animal Protocol Committee of Shanghai Jiao Tong University. Consent for publication Not applicable. Competing interests The authors declare no conflict of interest., (© 2024. The Author(s).)

Iodinated contrast material (ICM) is a critical component for many radiologic examinations and procedures. However, ICM has often been withheld in the past out of concern for its potential nephrotoxicity and increased risk of morbidity and mortality, often at the expense of diagnostic accuracy and timely diagnosis. Evidence from controlled studies now suggest that most cases of acute kidney injury (AKI) caused by ICM were instead due to contrast-independent causes of AKI or normal variation in renal function. This study will discuss current knowledge of contrast-induced AKI, including the incidence, sequelae, risk factors, and prevention strategies of this potential complication., Competing Interests: Disclosure J.S. McDonald and R.J. McDonald report investigator-initiated research grants with GE Healthcare, United Kingdom. J.S. McDonald and R.J. McDonald serve as consultants and scientific advisors for GE Healthcare regarding preclinical and clinical studies., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background and Aims: Contrast-associated acute kidney injury (CA-AKI) is a major complication following coronary procedures. We aimed to evaluate the effectiveness of a combination of urine flow rate-(UFR) guided hydration (RenalGuard TM ) and device-based contrast media (CM) reduction (DyeVert TM ) in CA-AKI prevention., Methods: Stable high-risk patients undergoing coronary procedures with the use of DyeVert TM and RenalGuard TM were prospectively included (Combined group) and matched with a similar cohort of patients treated only with RenalGuard TM in whom CM volume was controlled by operator-dependent strategies (Control group). CA-AKI was defined as a serum creatinine increase ≥0.3 mg/dL at 48 h., Results: Overall, 55 patients were enrolled and matched with comparable controls. Patients in the Combined group were exposed to a lower CM dose (Control: 55 [30-90] mL vs. Combined: 42.1 [24.9-59.4] mL; p = 0.024). A significant interaction was found between treatment allocation and serum creatinine changes (p = 0.048). CA-AKI occurred in five (9.1%) patients in the Combined group and in 14 (25.4%) patients in the Control group (OR 0.29, 95% CI [0.09-0.88])., Conclusions: A combined strategy of device-based CM reduction plus UFR-guided hydration is superior to operator-dependent CM sparing strategies plus UFR-guided hydration in preventing CA-AKI in high-risk patient., (© 2024 Wiley Periodicals LLC.)

Mitochondrial dysfunction and oxidative stress are involved in the development of contrast-induced acute kidney injury (CI-AKI). The present study aimed to reveal the role of transient receptor potential ankyrin 1 (TRPA1), an oxidative sensor, in CI-AKI. Trpa1 PT-/- mice with Trpa1 conditionally knocked out in renal proximal tubular (PT) cells, Trpa1 overexpression mice (Trpa1-OE), and TRPA1 agonists and antagonists were used to study its function in a mouse model of iohexol-induced CI-AKI. We found that TRPA1 was functionally expressed in PT cells. Activation of TRPA1 with cinnamaldehyde or overexpression of Trpa1 remarkably ameliorated renal tubular injury and dysfunction in a mouse model of CI-AKI, while CI-AKI was significantly exacerbated in Trpa1 PT-/- mice. Proteomics demonstrated that mouse kidneys with CI-AKI had downregulated proteins involved in mitochondrial dynamics and upregulated mitophagy-associated proteins. The beneficial effects of TRPA1 activation/overexpression on CI-AKI were associated with improved mitochondrial function, decreased mitochondrial fission and oxidative stress, enhanced mitophagy, and less apoptosis of renal tubular cells. TRPA1-induced decreases in mitochondrial fission were linked to upregulated fusion-related proteins (mitofusin 1, mitofusin 2 and optic atrophy 1) and downregulated fission mediator, phosphorylated dynamin-related protein 1 (Drp1). Importantly, inhibition of Drp1 with mitochondrial division inhibitor 1 improved CI-AKI. In addition, the decreased mitochondrial fission was also mediated by inactivation of AMP-activated protein kinase which mediates mitochondrial biogenesis. The findings suggest that TRPA1 plays a protective role in CI-AKI through regulating mitochondrial fission/fusion, biogenesis, and dysfunction. Activating TRPA1 may become novel therapeutic strategies for the prevention of CI-AKI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Contrast-associated acute kidney injury (CA-AKI) is a familiar complication following percutaneous coronary intervention (PCI). The present study evaluated the predictive value of the De Ritis ratio for CA-AKI and its association with long-term clinical outcomes in patients undergoing emergency PCI. Overall, 546 patients were included in this study. The De Ritis ratio was calculated by aspartate aminotransferase/alanine aminotransferase activity. The De Ritis ratios in the CA-AKI patients were significantly higher than the non-CA-AKI patients [3.74 (2.32, 4.90) vs 1.61 (1.02, 2.53); P < .001]. The De Ritis ratio was an independent risk factor for CA-AKI [odds ratio, 2.243; 95% confidence interval (CI), 1.823-2.759; P < .001]. The area under the ROC curve was .813 (95% CI, .763-.862; P < .001), and the sensitivity and specificity were 67.0% and 82.4%, respectively, when the optimum cut-off value was 2.97. Furthermore, patients in the high De Ritis ratio group (≥1.76) had a significantly greater incidence of primary endpoints [26.7% (73/273) vs 13.2% (36/273); P < .001], and the high De Ritis ratio was an independent predictor for primary endpoints (hazard ratio, 1.888, 95% CI, 1.235-2.887; P = .003). In conclusion, the De Ritis Ratio is associated with CA-AKI prediction and long-term clinical outcomes in patients undergoing emergency PCI., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Contrast-induced acute kidney injury (CI-AKI) is manifested by a rapid decline in renal function occurring within 48-72 h in patients exposed to iodinated contrast media (CM). Although intravenous hydration is currently the effective method confirmed to prevent CI-AKI, it has several drawbacks. Some investigations have demonstrated the nephroprotective effects of vagus nerve stimulation (VNS) against kidney ischemia-reperfusion injury, but no direct research has investigated the use of VNS for treating CI-AKI. Additionally, most current VNS treatment applies invasive electrical stimulator implantation, which is largely limited by the complications. Our recent publications introduce the magnetic vagus nerve stimulation (mVNS) system pioneered and successfully used for the treatment of myocardial infarction. However, it remains uncertain whether mVNS can mitigate CI-AKI and its specific underlying mechanisms. Therefore, we herein evaluate the potential therapeutic effects of mVNS on CM-induced nephropathy in rats and explore the underlying mechanisms., Results: mVNS treatment was found to significantly improve the damaged renal function, including the reduction of elevated serum creatinine (Scr), blood urea nitrogen (BUN), and urinary N-acetyl-β-D-glucosaminidase (NAG) with increased urine output. Pathologically, mVNS treatment alleviated the renal tissue structure injury, and suppressed kidney injury molecule-1 (KIM-1) expression and apoptosis in renal tubular epithelial cells. Mechanistically, increased circulating plasma exosomal miR-365-3p after mVNS treatment enhanced the autophagy and reduced CM-induced apoptosis in renal tubular epithelial cells by targeting Ras homolog enriched in brain (Rheb)., Conclusions: In summary, we demonstrated that mVNS can improve CI-AKI through enhanced autophagy and apoptosis inhibition, which depended on plasma exosomal miR-365-3p. Our findings highlight the therapeutic potential of mVNS for CI-AKI in clinical practice. However, further research is needed to determine the optimal stimulation parameters to achieve the best therapeutic effects., (© 2024. The Author(s).)

We developed a comprehensive kidney protection strategy (KPS), which comprises left ventricular end-diastolic pressure-guided saline hydration, ultralow contrast coronary angiography, and a staged coronary revascularization procedure under suitable conditions. This study aimed to investigate KPS's effect on the risk of developing contrast-associated acute kidney injury (CA-AKI) among persons with moderate-to-advanced kidney insufficiency (KI). Seventy patients who had undergone cardiac catheterization with an estimated glomerular filtration rate (eGFR) of 15-45 mL/min/1.73 m2 were investigated retrospectively. Among these, 19 patients who had received KPS and 51 who had undergone cardiac catheterization with usual care (UC) were enrolled. CA-AKI was defined as a 0.3-mg/dL increase in serum creatinine levels or dialysis initiation within 72 h after contrast exposure. The inverse probability of treatment weighting (IPTW)-adjusted cohort was analyzed according to the Mehran 2 risk categories. Patients' mean age was 73.3 ± 9.6 years; mean eGFR was 29.8 ± 8.5 mL/min/1.73 m2; and median of Mehran 2 risk score, 8. Most patients presented with acute myocardial infarction (AMI) or heart failure, and one-fifth of the administered cardiac catheterizations were emergency procedures. After the IPTW adjustment, the KPS group showed a significantly lower CA-AKI risk than the UC group (4% vs. 20.4%; odds ratio 0.19, 95% confidence interval 0.05-0.66). This effect was consistent across various subgroups according to different variables, including old age, AMI, advanced KI, high-risk category, left ventricular systolic dysfunction, and multivessel disease. Conclusively, KPS may reduce the CA-AKI risk in high-risk patients with moderate-to-advanced KI who have undergone cardiac catheterization., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Jong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

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.

The use of SGLT2 inhibitors (SGLT2is) has been found in large clinical studies to slow the progression of chronic kidney disease (CKD) and to lower the risk of acute kidney injury (AKI). Recent reports suggest that SGLT2is may also reduce the likelihood of developing radiocontrast-associated nephropathy (CAN) following contrast-enhanced imaging and intravascular interventions. This review underscores potential pitfalls and confounders in these studies and calls for caution in adopting their conclusions regarding the safety and renoprotective potency of SGLT2is, in particular in patients at high risk, with advanced CKD and hemodynamic instability undergoing coronary intervention. This caution is particularly warranted since both SGLT2is and contrast media intensify medullary hypoxia in the already hypoxic diabetic kidney and their combination may lead to medullary hypoxic damage, a principal component of CAN. Further studies are needed to evaluate this dispute, particularly in patients at high risk, and to reveal whether SGLT2is indeed provide renal protection or are hazardous during contrast-enhanced imaging and vascular interventions.

Although sodium-glucose transport protein-2 (SGLT2) inhibitors (SGLT2i) do not increase the risk of acute kidney injury (AKI) in general, they may pose a risk in patients undergoing angiography. This prospective cohort study aimed to evaluate the safety and efficacy of SGLT2i for post-contrast AKI (PC-AKI) in patients with type 2 diabetes mellitus (T2DM). Following screening, 306 patients with T2DM selected to undergo coronary arterial angiography with or without percutaneous intervention were enrolled. Patients were divided into the SGLT2i exposure and non-exposure groups. The primary outcome was PC-AKI, defined as an increase in serum creatinine levels > 0.5 mg/dL (44.2 µmol/L), or 25% above the baseline, within 48-72 h after exposure to contrast medium. The incidence of PC-AKI in the overall T2DM population was 5.2% (16/306). Following 1:1 propensity score matching, the incidence of PC-AKI was significantly higher in the SGLT2i group than in the non-SGLT2i group (10.7% vs. 2.9%; P = 0.027), with an odds ratio of 4.5 (95% confidence interval: 1.0-20.2; P = 0.047). Furthermore, PC-AKI occurred at a higher rate among short-term users of SGLT2i than long-term users (20.5% vs. 3.4%, P = 0.018). Thus, our findings suggest an increased risk of PC-AKI associated with short-term SGLT2i therapy in patients with T2DM., (© 2024. The Author(s).)

Background: Patients with chronic kidney disease and CAD have been denied revascularization because of fear of precipitating acute renal failure from contrast exposure. Skepticism on whether Ultra-Low contrast percutaneous coronary intervention (PCI) or Zero contrast PCI (ULC/ZC PCI) can be safely performed has limited its adoption., Methods: This observational registry enrolled 200 consecutive patients referred for elective PCI at a single center from June 2021 to December 2022. The study investigated whether the clinical outcomes of PCI performed with UL/ZC-PCI (n-48) were comparable to outcomes following standard PCI (n-152)., Results: Both groups were well matched in baseline and procedural characteristics. The groups had a highly statistical difference in the use of CV. Mean CV was 19.17 ± 7.29 cc in the ULC/ZC-group and 147.14 ± 73.55 cc in the control arm. The principal findings of the study were that the incidence of ontrast-induced acute kidney injury (AKI) was eightfold lower in patients receiving UL/ZC compared to the control group that received standard PCI. The incidence of all-cause mortality, myocardial infarction and major bleeding were similar in both groups. At 6 months, the decrement in renal function was lower in the group that received lower volumes of contrast., Conclusions: This single center observational registry demonstrated that UL-C/ZC-PCI is safe and effective in a broad spectrum of complex lesions. The skillsets needed to perform this are teachable, widely applicable and do not require a large upgrade of capital equipment. AKI rates and decrement in renal function at 6 months were both significantly lower in the UL-ZC group., (© 2024 Wiley Periodicals LLC.)

Contrast-induced acute kidney injury (CI-AKI) is a prevalent cause of renal dysfunction among hospitalized patients, yet the precise pathogenesis and effective therapeutic strategies remain elusive. In this study, we investigated the role of tubular ferroptosis in both experimental CI-AKI models and in primary tubular epithelial cells (PTECs) treated with ioversol. Using whole exome sequencing, we identified metallothioneins (MTs) as being among the most significantly downregulated genes following ioversol exposure. Our findings reveal that overexpression of Mt1 mitigates, whereas suppression of Mt-1 exacerbates, ioversol-induced tubular ferroptosis. Interestingly, the level of MTF1 (metal regulatory transcription factor 1), a principal regulator of Mt1, was found to increase in response to ioversol treatment. We further elucidated that ioversol activates LATS1 (Large tumor suppressor homolog 1), a kinase that promotes the phosphorylation and nuclear translocation of MTF1, thereby inhibiting its transcriptional activity for Mt1. Both genetic and pharmacological inhibition of LATS1 reversed the ioversol-induced suppression of Mt-1. From a therapeutic perspective, the LATS1 inhibitor TDI-011536, in combination with zinc acetate, was administered to a rodent model of CI-AKI. Our data indicate that this combination synergistically upregulates Mt1 expression and provides protection against contrast media-induced tubular ferroptosis. In summary, our study demonstrates that the reduction of Mt-1 contributes to tubular ferroptosis associated with CI-AKI. We show that contrast media activate LATS1, which in turn suppresses the transcriptional activity of MTF1 for Mt1. Herein, the combination of zinc acetate and a LATS1 inhibitor emerges as a potential therapeutic approach for the treatment of CI-AKI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Previous studies have reported a high occurrence of contrast-associated acute kidney injury (CA-AKI) in myocardial infarction (MI) patients undergoing primary percutaneous coronary intervention (PCI). However, the data on CA-AKI in MI patients who underwent elective PCI are limited. To evaluate the incidence of CA-AKI in MI patients undergoing elective PCI. The data were sourced from the Iodixanol-AKI Registry of MI patients scheduled to undergo elective PCI in 8 medical centers from May 2020 to November 2021. The participants were divided into three groups: acute, prior, and multiple MI. The outcomes measured were CA-AKI and the composite endpoint of major adverse renal and cardiovascular events (MARCE). The incidence of CA-AKI was 4.46% (37/830) in the MI patients, 4.40% (7/159) in the acute MI patients, 4.41% (22/499) in the prior MI patients, and 4.65% (8/172) in the multiple MI patients. Of note, 36 patients (97.30%) at AKI stage 1, and only 1 patient at AKI stage 2. There was no difference in the incidence of CA-AKI (P = 0.991) among the three groups. Multivariate regression analysis revealed that the independent risk factors for CA-AKI were diabetes and an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m 2 . MARCE occurred in 3.4% (28/830) of the total patients and was not associated with either any subgroup of patients with MI or AKI. The incidence of CA-AKI was low and mainly limited to mildly impaired renal function in MI patients undergoing elective PCI., (© 2024. The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI).)

The present study aimed to evaluate the predictive role of inflammatory biomarkers in the development of contrast-induced acute kidney injury (CI-AKI) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). The inflammatory biomarkers assessed were: platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), derived neutrophil-to-lymphocyte ratio (dNLR), neutrophil-to-lymphocyte*platelet ratio (NLPR), systemic inflammatory index (SII), and systemic inflammation response index (SIRI). Overall, 950 patients undergoing PCI were enrolled. The frequency of CI-AKI was 15.2% (n = 144). The levels of NLR, MLR, NLPR, SII, and SIRI were higher in the CI-AKI group than in the Non-CI-AKI group (P < .05). The addition of NLR ≥2.96, dNLR ≥2.08, NLPR ≥.012, SII ≥558.04, and SIRI ≥1.13 to the Mehran score model significantly increased the area under the curve (P < .05). Multivariable logistic regression analyses indicated that inflammatory biomarkers were significantly associated with CI-AKI, including NLR ≥2.96 (OR = 1.588, P = .017), dNLR ≥2.08 (OR = 1.686, P = .007), SII ≥558.04 (OR = 1.521, P = .030), and SIRI ≥1.13 (OR = 1.601, P = .017). Therefore, inflammation is associated with the development of CI-AKI, and preoperative hematological inflammatory markers could predict the risk of CI-AKI in ACS patients undergoing PCI., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

With the increasing incidence of coronary heart disease (CHD), contrast-associated nephropathy (CAN) caused by contrast agents required in coronary angiography has gradually become a clinical concern that needs to be solved urgently. At present, CAN has become one of the most common causes of hospital-acquired acute kidney injury, which seriously affects the prognosis and health of patients. How to effectively identify high-risk CAN patients and prevent the occurrence of CAN has become a hotspot of clinical research. In this study, we attempted to evaluate the effect of contrast agents on renal injury in diabetes mellitus (DM) and non-DM patients by observing some indexes of early renal injury and inflammatory factors, so as to provide a more comprehensive reference for early identification of CAN in the future. The results showed that compared with non-DM patients, contrast agents caused more obvious renal damage in DM patients and more significantly activated inflammatory responses, increasing the risk of CAN. Cystatin C (CysC), neutrophil gelatinase-associated lipocalin (NGAL), C-reactive protein (CRP), and neutrophil-lymphocyte ratio (NLR) all showed excellent predictive effects for the occurrence of CAN after coronary angiography in both DM and non-DM patients.

Purpose: The purpose of the study was to explore the predictive value of free triiodothyronine to free thyroxine ratio (FT3/FT4) on contrast-associated acute kidney injury (CA-AKI) and poor prognosis in euthyroid patients after percutaneous coronary intervention (PCI)., Methods: The present study included 3,116 euthyroid patients who underwent elective PCI. The main outcome was CA-AKI, and the secondary outcome was long-term mortality. All patients were divided into three groups according to the tertiles of FT3/FT4 levels., Results: During hospitalization, a total of 160 cases (5.1%) of CA-AKI occurred. Restricted cubic spline (RCS) analysis indicated a linear and negative relationship between FT3/FT4 and CA-AKI risk (P for nonlinearity = 0.2621). Besides, the fully-adjusted logistic regression model revealed that patients in tertile 3 (low FT3/FT4 group) had 1.82 times [odds ratio (OR): 1.82, 95% confidence interval (CI): 1.13-3.02, P = 0.016] as high as the risk of CA-AKI than those in tertile 1 (high FT3/FT4 group). Similarly, patients in tertile 3 were observed to have a higher incidence of long-term mortality [fully-adjusted hazard ratio (HR): 1.58, 95% CI: 1.07-2.32, P = 0.021]. Similarly, the Kaplan-Meier curves displayed significant differences in long-term mortality among the three groups (log-rank test, P < 0.001)., Conclusion: In euthyroid patients undergoing elective PCI, low levels of FT3/FT4 were independently associated with an increased risk of CA-AKI and long-term mortality. Routine evaluation of FT3/FT4 may aid in risk stratification and guide treatment decisions within this particular patient group., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Purpose: To investigate the renal pathophysiological processes and protective effect of quercetin on contrast-induced acute kidney injury (CI-AKI) in mice with type 1 diabetic mellitus(DM) using diffusion tensor imaging(DTI). Methods: Mice with DM were divided into two groups. In the diabetic + contrast medium(DCA) group, the changes of the mice kidneys were monitored at 1, 24, 48, and 72 h after the injection of iodixanol(4gI/kg). The mice in the diabetic + contrast medium + quercetin(DCA + QE) group were orally given different concentrations of quercetin for seven days before injection of iodixanol. In vitro experiments, renal tubular epithelial (HK-2) cells exposed to high glucose conditions were treated with various quercetin concentrations before treatment with iodixanol(250 mgI/mL). Results: DTI-derived mean diffusivity(MD) and fractional anisotropy(FA) values can be used to evaluate CI-AKI effectively. Quercetin significantly increased the expression of Sirt 1 and reduced oxidative stress by increasing Nrf 2/HO-1/SOD1. The antiapoptotic effect of quercetin on CI-AKI was revealed by decreasing proteins level and by reducing the number of apoptosis-positive cells. In addition, flow cytometry indicated quercetin-mediated inhibition of M1 macrophage polarization in the CI-AKI. Conclusions: DTI will be an effective noninvasive tool in diagnosing CI-AKI. Quercetin attenuates CI-AKI on the basis of DM through anti-oxidative stress, apoptosis, and inflammation.

Background: The systemic inflammatory response index (SIRI), served as a novel inflammatory biomarker, is the synthesis of neutrophils, monocytes and lymphocytes., Aims: We hypothesized that SIRI has predictive value for contrast-associated acute kidney injury (CA-AKI) and long-term mortality in patients undergoing elective percutaneous coronary intervention (PCI)., Methods: We retrospectively observed 5685 patients undergoing elective PCI from January 2012 to December 2018. Venous blood samples were collected to obtain the experimental data on the day of admission or the morning of the next day. SIRI = neutrophil count × monocyte count/lymphocyte count. CA-AKI was defined as an increase of 50% or 0.3 mg/dl in SCr from baseline within 48 h after contrast exposure., Results: The incidence of CA-AKI was 6.1% ( n  = 352). The best cutoff value of SIRI for predicting CA-AKI was 1.39, with a sensitivity of 52.3% and a specificity of 67.3%. [AUC: 0.620, 95% confidence interval (CI): 0.590-0.651, p  < 0.001]. After adjusting for potential confounders, multivariate analysis showed that the high SIRI group (SIRI > 1.39) was a strong independent predictor of CA-AKI in patients undergoing elective PCI compared with the low SIRI group (SIRI ≤ 1.39) (odds ratio = 1.642, 95% CI: 1.274-2.116, p <  0.001). Additionally, COX regression analysis showed that SIRI > 1.39 was significantly associated with long-term mortality at a median follow-up of 2.8 years. [Hazard ratio (HR)=1.448, 95%CI: 1.188-1.765; p  < 0.001]. Besides, Kaplan-Meier survival curve also indicated that the cumulative rate of mortality was considerably higher in the high SIRI group., Conclusions: High levels of SIRI are independent predictors of CA-AKI and long-term mortality in patients undergoing elective PCI.

Purpose: To investigate the relationship between contrast medium administration and long-term mortality and renal function in patients with septic acute kidney injury (AKI)., Materials and Methods: We performed a retrospective, propensity-matched cohort study involving 1521 adult patients admitted with septic shock. Patients with septic AKI who underwent contrast or non-contrast CT scans were enrolled. The primary outcomes were the rates of 90-day mortality and dialysis within 90 days. The secondary outcomes included worsening of AKI, in-hospital mortality, and maintenance of dialysis after 90 days., Results: During the study period, 609 patients with septic AKI were identified; 220 (36.1%) underwent contrast CT and 389 (63.9%) underwent non-contrast CT. After propensity score matching, 133 pairs were obtained. There were no significant differences between the contrast and non-contrast CT groups in 90-day mortality (54.9% vs. 58.6%, P = 0.579), dialysis within 90 days (6.8% vs. 8.3%, P = 0.655), worsening AKI (2.3% vs. 3.0%, P = 0.706), in-hospital mortality (10.6% vs. 14.4%, P = 0.369), or maintenance of dialysis after 90 days (0.0% vs. 0.8%, P > 0.99)., Conclusions: The administration of intravenous contrast medium was not associated with long-term mortality, deterioration of renal function, or dialysis in patients with septic AKI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: This study aimed to elucidate the association between IV contrast media CT and acute kidney injury (AKI) and in-hospital mortality among patients requiring emergency admission., Design: In this retrospective observational study, we examined AKI within 48 hours after CT, renal replacement therapy (RRT) dependence at discharge, and in-hospital mortality in patients undergoing contrast-enhanced CT or nonenhanced CT. We performed 1:1 propensity score matching to adjust for confounders in the association between IV contrast media use and outcomes. Subgroup analyses were performed according to age, sex, diagnosis at admission, ICU admission, and preexisting chronic kidney disease (CKD)., Setting and Patients: This study used the Medical Data Vision database between 2008 and 2019. This database is Japan's largest commercially available hospital-based claims database, covering about 45% of acute-care hospitals in Japan, and it also records laboratory results., Interventions: None., Measurements and Main Results: The study included 144,149 patients with (49,057) and without (95,092) contrast media exposure, from which 43,367 propensity score-matched pairs were generated. Between the propensity score-matched groups of overall patients, exposure to contrast media showed no significant risk of AKI (4.6% vs. 5.1%; odds ratio [OR], 0.899; 95% CI, 0.845-0.958) or significant risk of RRT dependence (0.6% vs. 0.4%; OR, 1.297; 95% CI, 1.070-1.574) and significant benefit for in-hospital mortality (5.4% vs. 6.5%; OR, 0.821; 95% CI, 0.775-0.869). In subgroup analyses regarding preexisting CKD, exposure to contrast media was a significant risk for AKI in patients with CKD but not in those without CKD., Conclusions: In this large-scale observational study, IV contrast media was not associated with an increased risk of AKI but concurrently showed beneficial effects on in-hospital mortality among patients requiring emergency admission., Competing Interests: The authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

Background: Iodinated contrast-induced acute kidney injury (CI-AKI) is a common cause of renal failure, especially in patients with risk factors. This study analyses different renal biomarkers in patients undergoing computed tomography scans with iodinated contrast to identify the molecular and cellular mechanisms involved in the pathogenesis of CI-AKI., Methodology: Prospective study that included patients with high risk of renal disease who received iodinated contrast (iohexol) for the computed tomography scans. Functional biomarkers (creatinine and cystatin C), inflammatory and oxidative stress markers (neutrophil gelatinase-associated lipocalin [NGAL], interleukin-8 [IL-8], superoxide dismutase [SOD], F2-isoprostanes, and cardiotrophin-1), and cell cycle biomarkers (Nephrocheck®) were analysed before the iodinated contrast and 4, 12, 24, and 48 hours post-contrast, in relation to the incidence of IC-AKI., Results: IC-AKI was observed in 30.6% of the 62 study participants and in 57.1% of the patients with diabetes and renal dysfunction. Factors associated with IC-AKI were a higher mean age (74.4 vs 64.9 years), pre-existing renal dysfunction (60 vs 16.7%), and higher adjusted mean volume of iohexol (42.9 vs 32.1%). As for non-functional biomarkers. No differences were found between patients with and without CI-AKI. The use of iodinated contrast was associated with a decrease in SOD antioxidant activity at 4 hours and an increase in IL-8 at 12 hours post-administration of the iodinated contrast., Conclusions: Administration of iohexol in computed tomography scans in patients with high risk of renal disease results in an elevated percentage of CI-AKI, attributable to ischemia/reperfusion injury and/or direct toxicity of the iodinated contrast.

Although community-acquired acute kidney injury (CA-AKI) represents a significant subset of all AKI incidence, evidence is limited due to the lack of comprehensive data prior to diagnosis. Here, we examined the risk of drug use for CA-AKI by using exhaustive pre-diagnostic prescription data. We included 78,754 working-age healthy individuals who underwent an annual health checkup program. We conducted a cohort study to assess the association between prevalent drug use and subsequent CA-AKI incidence using the Cox proportional hazard model. Subsequently, we conducted a case-crossover study to compare the new drug use in the case period directly before the CA-AKI incidence (- 3 to 0 months) with that in the control period far before the CA-AKI incidence (- 15 to - 12 months and - 9 to - 6 months) using the conditional Poisson regression model. The prevalent use of renin-angiotensin-aldosterone system (RAAS) inhibitors was associated with an increased CA-AKI incidence, but the new use was not. The new use of diuretics, anti-infectious drugs, and contrast medium was also associated with an increased CA-AKI incidence. These results suggest we need to pay attention for the incidence of AKI among the general population taking those common drugs., (© 2024. The Author(s).)

Purpose of the Review: Contrast-associated acute kidney injury (CA-AKI) remains a significant concern in diagnostic and invasive procedures, particularly in the context of iodinated contrast material administration. The traditional definition of CA-AKI, based on serum creatinine elevation following contrast exposure, may not accurately capture its multifactorial nature., Recent Findings: Studies have provided new insights into the differential incidence of CA-AKI between intravenous and intraarterial contrast administration, emphasizing the importance of tailored preventative strategies for high-risk procedures. This higher risk may arise from two proposed mechanisms: one implicating free radical formation leading to cytotoxicity and apoptosis in renal cells and another suggesting that contrast media alter renal hemodynamics, particularly in the outer medulla, by constricting the vasa recta and reducing medullary flow. Advances in technology and patient care, including contemporary use of low-osmolar contrast agents and hydration protocols, mitigate CA-AKI risk. Diagnostic and invasive procedures should not be avoided solely due to concerns about renal dysfunction if the patient is likely to benefit clinically., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: In April of 2022, the COVID-19 pandemic resulted in a global shortage of intravenous contrast media (ICM), which led our health care system to implement rationing measures., Study Objectives: We set out to determine if the reduction in ICM use was associated with a change in the incidence of acute kidney injury (AKI)., Methods: We conducted a multicenter retrospective cohort analysis to compare the incidence of AKI in patients who presented before and after ICM rationing. Adult patients who had a CT of the abdomen performed who had at least 2 creatinine measurements, at least 24 h apart, were included. The maximum increase in creatinine was determined by subtracting the maximal creatinine obtained within 7 days with the initial creatinine. The primary outcome was the development of AKI., Results: A total of 2168 patients met inclusion criteria (1082 before; 1086 after). There was no significant difference in age, gender, comorbid conditions, disposition, or initial estimated glomerular filtration rate between groups. In the prerationing group, 87.7% of patients received ICM compared to 42.7% after. There was no significant difference in the development of AKI between groups (11.1% vs. 11.0%), including when stratified by baseline renal function and adjusted for age, sex, race, comorbid conditions, and emergency severity index., Conclusions: The dramatic reduction in ICM use that resulted from the global shortage was not associated with a change in the incidence of AKI. This reinforces the results of previous studies which have failed to find evidence of a relationship between ICM administration and AKI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

The aim of the present study was to define the risk factors associated with contrast-induced acute kidney injury (CI-AKI) in patients who underwent coronary artery angiography (CAG). In this retrospective cohort study, patients who underwent CAG between March 2014 and January 2022 were evaluated. A total of 2923 eligible patients were included in the study. Univariate and multivariate logistic regression analysis was used to identify the predictive factors. CI-AKI developed in 77 (2.6%) of 2923 patients. In multivariate analysis, diabetes mellitus (DM), chronic kidney disease (CKD), and estimated glomerular filtration rate (eGFR) were found to be independent factors associated with CI-AKI. In the subgroup analysis of patients with eGFR ≥60 mL/min/1.73 m 2 , eGFR remained a predictor of CI-AKI (Odds ratio (OR): .89, 95% CI: .84-.93; that is, a lower eGFR remains a risk factor for CI-AKI). In the receiving operating characteristic (ROC) analysis of patients with eGFR ≥60 mL/min/1.73 m 2 , the area under the curve of the eGFR was .826. Using the ROC curve based on Youden's index, the eGFR cut-off was found to be 70 mL/min/1.73 m 2 for patients with eGFR ≥60 mL/min/1.73 m 2 . eGFR is also an important risk factor in patients with eGFR 60-70 mL/min/1.73 m 2 ., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Contrast-induced acute kidney injury (CI-AKI) is an acute renal complication that occurs after intravascular contrast agent administration. Sodium selenite (SS) is an inorganic source of Se and has potent antioxidant properties. This study intends to examine its anti-inflammatory and antioxidant effects in CI-AKI., Methods: A rat CI-AKI model was established with the pretreatment of SS (0.35 mg/kg). Hematoxylin-eosin staining was employed for histopathological analysis of rat kidney specimens. Biochemical analysis was conducted for renal function detection. Tissue levels of oxidative stress-related markers were estimated. Reverse transcription-quantitative polymerase chain reaction revealed the mRNA levels of proinflammatory cytokines. Western blotting showed the Nrf2 signaling-related protein expression in the rat kidney., Results: SS administration alleviated the renal pathological changes and reduced the serum levels of serum creatinine, blood urea nitrogen, neutrophil gelatinase-associated lipocalin, cystatin C, and urinary level of kidney injury molecule-1 in CI-AKI rats. SS attenuated oxidative stress and inflammatory response in CI-AKI rat kidney tissues. SS activated the Nrf2 signaling transduction in the renal tissues of rats with CI-AKI., Conclusion: SS ameliorates CI-AKI in rats by reducing oxidative stress and inflammation via the Nrf2 signaling., (© 2024. The Author(s).)

Objectives: This study aimed to identify the incidence and risk factors for contrast-associated acute kidney injury nephropathy (CA-AKI) in patients undergoing contrast-enhanced computed tomography (CCT) in the emergency department., Materials and Methods: In this retrospective single-center study, patients aged 18 and older who visited the emergency department and underwent CCT between January and February 2022 were included. The Mehran score, calculated from patient data, was used to assess risk. CA-AKI development was determined by measuring serum creatinine (SCr) levels 48-72 h post-contrast administration., Results: The study included 532 patients, with a mean age of 57 ± 19 years; 53.2% were male. CA-AKI developed in 16% of cases, 5.82% required hemodialysis, and 7.9% died. The Mehran score was the only significant predictor of CA-AKI development. Patients with a Mehran score of 16 or higher had a 161-fold increased risk of developing CA-AKI compared to those with a score of 5 or lower. The model achieved a 91.3% correct classification rate. Logistic regression analysis showed that CA-AKI significantly increased mortality risk by 15.7 times., Conclusion: The Mehran score, originally developed for predicting CA-AKI risk post-coronary intervention, is also effective for predicting CA-AKI risk after CCT. While CA-AKI is a significant factor affecting mortality, it is not the sole cause of death (Nagelkerke R2 value 0.310).

Percutaneous coronary intervention (PCI) is a crucial diagnostic and therapeutic approach for coronary heart disease. Contrast agents' exposure during PCI is associated with a risk of contrast-induced acute kidney injury (CI-AKI). CI-AKI is characterized by a sudden decline in renal function occurring as a result of exposure to intravascular contrast agents, which is associated with an increased risk of poor prognosis. The pathophysiological mechanisms underlying CI-AKI involve renal medullary hypoxia, direct cytotoxic effects, endoplasmic reticulum stress, inflammation, oxidative stress, and apoptosis. To date, there is no effective therapy for CI-AKI. High-mobility group box 1 (HMGB1), as a damage-associated molecular pattern molecule, is released extracellularly by damaged cells or activated immune cells and binds to related receptors, including toll-like receptors and receptor for advanced glycation end product. In renal injury, HMGB1 is expressed in renal tubular epithelial cells, macrophages, endothelial cells, and glomerular cells, involved in the pathogenesis of various kidney diseases by activating its receptors. Therefore, this review provides a theoretical basis for HMGB1 as a therapeutic intervention target for CI-AKI., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

The risk of acute renal failure (ARF) following iodinated contrast media injection has long been overestimated because of the previous use of more toxic ICPs and uncontrolled studies. Nowadays, this concept is being questioned. Patients with severe renal failure and/or ARF are the only group still considered at risk. In these patients, it is necessary to discuss an alternative without an iodinated contrast agent. Contrast-enhanced ultrasound, MRI, spectral CT or PET-CT scan can be used instead of contrast-enhanced CT. Preventive measures should be applied when appropriate substitute to CT is not available or not diagnosed (minimum necessary dose of ICP, interruption of some treatments and prior hydration). These recommendations formalized by the European Society of Urogenital Radiology (ESUR) in 2018 address most situations faced by clinicians. In complex situations, an opinion from a nephrologist remains necessary after asking the radiologist about the availability of acceptable substitutes., (Copyright © 2022 Société Française du Cancer. Published by Elsevier Masson SAS. All rights reserved.)

Iodinated contrast material (ICM) has revolutionized the field of diagnostic radiology through improvements in diagnostic performance and the expansion of clinical indications for radiographic and CT examinations. Historically, nephrotoxicity was a feared complication of ICM use, thought to be associated with a significant risk of morbidity and mortality. Such fears often precluded the use of ICM in imaging evaluations, commonly at the expense of diagnostic performance and timely diagnosis. Over the past 20 years, the nephrotoxic risk of ICM has become a topic of debate, as more recent evidence from higher-quality studies now suggests that many cases of what was considered contrast-induced acute kidney injury (CI-AKI) likely were cases of mistaken causal attribution; most of these cases represented either acute kidney injury (AKI) caused by any of myriad other known factors that can adversely affect renal function and were coincidentally present at the time of contrast media exposure (termed "contrast-associated AKI" [CA-AKI]) or a manifestation of the normal variation in renal function that increases with worsening renal function. This Special Series Review discusses the current state of knowledge regarding CI-AKI and CA-AKI, including the incidence, risk factors, outcomes, and prophylactic strategies in the identification and management of these clinical conditions.

Objectives: To compare the risk of acute kidney injury (AKI) between hospitalized children who received intravenous contrast media for imaging examinations and those who did not., Methods: This retrospective cohort study enrolled patients aged 0-18 years with serum creatinine levels before and after imaging examinations from 2015 to 2020 at Beijing Children's Hospital. Participants were classified into an exposure group or a control group. Log-binomial regression analysis was used to estimate the adjusted risk ratio (aRR) value for the association between exposure to contrast media and consequential AKI. After which, inverse probability treatment weighting was used to reduce systematic differences in baseline characteristics among the groups. Moreover, subgroup and sensitivity analyses were performed. Finally, multivariate logistic regression analysis was performed to identify risk factors for pediatric AKI., Results: In total, 3061 pediatric patients were included in the analyses (median age, 4.5 [IQR, 1.3-8.9] years, 1760 males). According the KDIGO definition of AKI, the incidence of AKI in the exposure group, and the control group were 7.4% and 6.5%, respectively; furthermore, the aRR was 1.35 (95% CI: 1.31-1.39). In patients underwent CT, the risk of AKI in the exposure group of contrast media increased compared with the control group and the aRR was 1.39 (95% CI: 1.09-1.78). However, it is not observed in patients underwent MRI (aRR: 1.36; 95% CI: 0.96-1.95). According to our subgroup analysis of pediatric patients aged ≥ 2 years (aRR: 1.38; 95% CI: 1.05-1.82) and sensitivity analysis (aRR: 1.32, 95% CI: 1.08-1.61), the risk of AKI in the exposure group was greater than that in the control group. An increased risk to exposure to contrast media was seen in females (aRR: 1.41, 95% CI: 1.05-1.89) rather than males (aRR: 1.30, 95% CI: 0.99-1.70). According to the multivariate logistic regression analyses, the baseline eGFR (OR: 1.02; 95% CI: 1.01-1.03) and comorbidities (OR: 2.97; 95% CI: 1.89-4.65) were risk factors, while age (OR: 0.87; 95% CI: 0.84-0.91) was a protective factor against AKI., Conclusion: The evidence from the present study suggested that the increased risk of AKI in hospitalized children induced by intravascular contrast should not be ignored., (© 2024. The Author(s).)

Purpose: Both glucose and albumin are associated with chronic inflammation, which plays a vital role in post-contrast acute kidney injury (PC-AKI). To explore the relationship between random glucose to albumin ratio (RAR) and the incidence of PC-AKI after percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI)., Patients and Methods: STEMI patients who underwent PCI were consecutively enrolled from January, 01, 2010 to February, 28, 2020. All patients were categorized into T1, T2, and T3 groups, respectively, based on RAR value (RAR < 3.377; 3.377 ≤ RAR ≤ 4.579; RAR > 4.579). The primary outcome was the incidence of PC-AKI, and the incidence of major adverse clinical events (MACE) was the second endpoint. The association between RAR and PC-AKI was assessed by multivariable logistic regression analysis., Results: A total of 2,924 patients with STEMI undergoing PCI were finally included. The incidence of PC-AKI increased with the increasing tertile of RAR (3.2% vs 4.8% vs 10.6%, P<0.001). Multivariable regression analysis demonstrated that RAR (as a continuous variable) was associated with the incidence of PC-AKI (adjusted odds ratio (OR) =1.10, 95% confidence interval (CI) =1.04 - 1.16, P<0.001) and in-hospital MACE (OR=1.07, 95% CI=1.02 - 1.14, P=0.012); RAR, as a categorical variable, was significantly associated with PC-AKI (T3 vs. T1, OR=1.70, 95% CI=1.08 - 2.67, P=0.021) and in-hospital MACE (T3 vs. T1, OR=1.63, 95% CI=1.02 - 2.60, P=0.041) in multivariable regression analyses. Receiver operating characteristic curve analysis showed that RAR exhibited a predictive value for PC-AKI (area under the curve (AUC)=0.666, 95% CI=0.625 - 0.708), and in-hospital MACE (AUC= 0.662, 95% CI =0.619 - 0.706)., Conclusions: The high value of RAR was significantly associated with the increasing risk of PC-AKI and in-hospital MACE after PCI in STEMI patients, and RAR offers a good predictive value for those outcomes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Lai, Gu, Lin, He, Dai, Duan, Liu and He.)

Objective: To investigate the effect of Dapagliflozin, sodium-glucose cotransporter 2 inhibitor (SGLT2i), on contrast-induced acute kidney injury (CIAKI) in patients with type 2 diabetes mellitus (T2DM) after percutaneous coronary intervention(PCI). Methods: A cohort study . The clinical data of 366 patients with coronary heart disease combined with T2DM who underwent PCI in the Department of Cardiology, Tianjin University Chest Hospital, from June 2021 to June 2022 were retrospectively analyzed, including 218 males and 148 females, aged (64.6±11.0) years old. According to whether the patients had used Dapagliflozin or not, the selected patients were divided into SGLT2i group( n =124) and control group( n =242). The changes in cardiac indicators, renal function, and inflammatory response indicators before and 72 hours after PCI treatment were analyzed and compared between the two groups. The incidence rate of CIAKI in the two groups was analyzed, and the influencing factors of CIAKI were analyzed by multivariate logistic regression. The major adverse cardiac events (MACE) were recorded during the follow-up period of the two groups, and Kaplan-Meier survival analysis and log-rank test were used to compare the differences in MACE occurrence between the two group. Results: The left ventricular ejection fraction (LVEF) of the SGLT2i group was lower than that of the control group, and the proportion of patients with LVEF<45% and CIAKI risk score were higher than those of the control group, with statistical significance (all P <0.05). 72 h after PCI treatment, β-2 Microglobulin(β-2MG), cystatin-C(Cys-C), and neutrophil gelatinase-associated lipocalin (NGAL) in both groups were all increased compared to those before PCI treatment, with statistical significance (all P <0.05).β-2MG, Cys-C, and NGAL in SGLT2i group were all lower than those in the control group, with statistical significance(all P <0.05).The levels of interleukin-6(IL-6), hypersensitive C-reactive protein (hs-CRP), and malondialdehyde in both groups of patients increased compared to preoperative levels, while the levels of superoxide dismutase (SOD) decreased compared to preoperative levels, with statistical significance (all P <0.05). The levels of IL-6, hs-CRP, and malondialdehyde in the SGLT2i group were lower than those in the control group, while SOD was higher than that in the control group, with statistical significance (all P <0.05). Among all patients included, 34 cases experienced CIAKI (9.8%), and the incidence of CIAKI in the SGLT2i group was lower than that in the control group [4.8% (6/124) vs 11.6% (28/242), P =0.037]. Multivariate logistic regression analysis showed that the use of dapagliflozin was a protective factor for CIAKI in T2DM patients receiving PCI treatment ( OR =0.321, 95% CI : 0.127-0.816, P =0.017). After a follow-up of 14.0 (12.0, 16.2) months, the incidence of MACE in SGLT2i group was lower than that in the control group (7.3% vs 12.8%, P =0.048). Conclusions: Dapagliflozin may reduce the risk of CIAKI and MACE in T2DM patients after PCI treatment. Its mechanism may be related to the anti-inflammatory and antioxidant effects of SGLT2i.

Objective: Contrast media (CM) is a commonly applied drug in medical examination and surgery. However, contrast-induced acute kidney injury (CIAKI) poses a severe threat to human life and health. Notably, the CUT-like homeobox 1 (CUX1) gene shows protective effects in a variety of cells. Therefore, the objective of this study was to provide a new target for the treatment of CIAKI through exploring the role and possible molecular mechanism of CUX1 in CIAKI., Method: Blood samples were collected from 20 patients with CIAKI and healthy volunteers. Human kidney 2 (HK-2) cells were incubated with 200 mg/mL iohexol for 6 h to establish a contrast-induced injury model of HK-2 cells. Subsequently, qRT-PCR was used to detect the relative mRNA expression of CUX1; CCK-8 and flow cytometry to assess the proliferation and apoptosis of HK-2 cells; the levels of IL(interleukin)-1β, tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA) in cells and lactate dehydrogenase (LDH) activity in cell culture supernatant were detect; and western blot to observe the expression levels of CUX1 and the PI3K/AKT signaling pathway related proteins [phosphorylated phosphoinositide 3-kinase (p-PI3K), PI3K, phosphorylated Akt (p-AKT), AKT]., Results: CUX1 expression was significantly downregulated in blood samples of patients with CIAKI and contrast-induced HK-2 cells. Contrast media (CM; iohexol) treatment significantly reduced the proliferation of HK-2 cells, promoted apoptosis, stimulated inflammation and oxidative stress that caused cell damage. CUX1 overexpression alleviated cell damage by significantly improving the proliferation level of HK-2 cells induced by CM, inhibiting cell apoptosis, and reducing the level of LDH in culture supernatant and the expression of IL-1β, TNF-α and MDA in cells. CM treatment significantly inhibited the activity of PI3K/AKT signaling pathway activity. Nevertheless, up-regulating CUX1 could activate the PI3K/AKT signaling pathway activity in HK-2 cells induced by CM., Conclusion: CUX1 promotes cell proliferation, inhibits apoptosis, and reduces inflammation and oxidative stress in CM-induced HK-2 cells to alleviate CM-induced damage. The mechanism of CUX1 may be correlated with activation of the PI3K/AKT signaling pathway., (© 2024. The Author(s).)

Background: Acute kidney injury (AKI) after transcatheter aortic valve implantation (TAVI) is a serious complication which is associated with increased mortality. The RenalGuard system was developed to reduce the risk of AKI after contrast media exposition by furosemide-induced diuresis with matched isotonic intravenous hydration. The aim of this study was to examine the effect of the RenalGuard system on the occurrence of AKI after TAVI in patients with chronic kidney disease., Methods: The present study is a single-center randomized trial including patients with severe aortic valve stenosis undergoing TAVI. Overall, a total of 100 patients treated by TAVI between January 2017 and August 2018 were randomly assigned to a periprocedural treatment with the RenalGuard system or standard treatment by pre- and postprocedural intravenous hydration. Primary endpoint was the occurrence of AKI after TAVI, and secondary endpoints were assessed according to valve academic research consortium 2 criteria., Results: Overall, the prevalence of AKI was 18.4% (n = 18). The majority of these patients developed mild AKI according to stage 1. Comparing RenalGuard to standard therapy, no significant differences were observed in the occurrence of AKI (RenalGuard: 21.3%; control group: 15.7%; p = 0.651). In addition, there were no differences between the groups with regard to 30-day and 12-month mortality and procedure-associated complication rates., Conclusion: In this randomized trial, we did not detect a reduction in AKI after TAVI by using the RenalGuard system. A substantial number of patients with chronic kidney disease developed AKI after TAVI, whereas the majority presented with mild AKI according to stage 1 (ClinicalTrials.gov number NCT04537325)., (© 2023. The Author(s).)

Purpose: Acute kidney injury (AKI) is a common early complication secondary to transcatheter aortic valve replacement (TAVR). Studies on the incidence and risk factors for AKI after TAVR surgery are limited to date. Here, we retrospectively analyzed the incidence and risk factors for AKI after TAVR surgery in our hospital., Materials and Methods: Patients who underwent TAVR surgery at our hospital from November 2017 to February 2023 were selected. AKI was defined using the 2012 KDIGO definition and staging criteria. The relevant data and information between the AKI group and the non-AKI group were compared and analyzed, and a binary logistic regression model was used to analyze the risk factors for AKI., Results: A total of 75 patients who underwent TAVR surgery were included in the retrospective analysis. After TAVR, the incidence of AKI was 17.3% (13/75), of which 8 (61.5%) had stage 1 AKI, 2 (15.4%) had stage 2 AKI, 3 (23.1%) had stage 3 AKI, and 3 needed renal replacement therapy. After multivariate logistic analysis, contrast volume (OR = 1.024 (1.001, 1.047)) was found to be an independent risk factor for AKI, while patients with high estimated glomerular filtration rate (eGFR) (OR = 0.903 (0.826, 0.986)) have a reduced risk of AKI., Conclusion: A retrospective study revealed a 17.3% incidence of AKI after TAVR surgery in our hospital, most of which were stage 1 AKI. A low preoperative eGFR and contrast volume were found to be independent risk factors for AKI.

Acute kidney injury (AKI) is a critical complication known for their extremely high mortality rate and lack of effective clinical therapy. Disorders in mitochondrial dynamics possess a pivotal role in the occurrence and progression of contrast-induced nephropathy (CIN) by activating NLRP3 inflammasome. The activation of dynamin-related protein-1 (Drp1) can trigger mitochondrial dynamic disorders by regulating excessive mitochondrial fission. However, the precise role of Drp1 during CIN has not been clarified. In vivo experiments revealed that inhibiting Drp1 through Mdivi-1 (one selective inhibitor of Drp1) can significantly decrease the expression of p-Drp1 (Ser616), mitochondrial p-Drp1 (Ser616), mitochondrial Bax, mitochondrial reactive oxygen species (mROS), NLRP3, caspase-1, ASC, TNF-α, IL-1β, interleukin (IL)-18, IL-6, creatinine (Cr), malondialdehyde (MDA), blood urea nitrogen (BUN), and KIM-1. Moreover, Mdivi-1 reduced kidney pathological injury and downregulated the interaction between NLRP3 and thioredoxin-interacting protein (TXNIP), which was accompanied by decreased interactions between TRX and TXNIP. This resulted in increasing superoxide dismutase (SOD) and CAT activity, TRX expression, up-regulating mitochondrial membrane potential, and augmenting ATP contents and p-Drp1 (Ser616) levels in the cytoplasm. However, it did not bring impact on the expression of p-Drp1 (Ser637) and TXNIP. Activating Drp-1though Acetaldehyde abrogated the effects of Mdivi-1. In addition, the results of in vitro studies employing siRNA-Drp1 and plasmid-Drp1 intervention in HK-2 cells treated with iohexol were consistent with the in vivo experiments. Our findings revealed inhibiting Drp1 phosphorylation at Ser616 could ameliorate iohexol -induced acute kidney injury though alleviating the activation of the TXNIP-NLRP3 inflammasome pathway., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: The link between malnutrition and poor prognosis in cardiovascular disease has been established but the association between malnutrition and contrast-associated acute kidney injury (CA-AKI), a common complication of coronary procedures, remains poorly understood. In this study we investigated the predictive value of 3 nutritional indexes for CA-AKI in patients undergoing percutaneous coronary intervention (PCI)., Methods and results: The study included a total of 6,049 consecutive patients undergoing PCI between May 2012 and September 2020, among whom 352 (5.8%) developed CA-AKI. We used the Controlling Nutritional Status (CONUT) score, the Geriatric Nutritional Risk Index (GNRI), and the Prognostic Nutritional Index (PNI) to assess the association between malnutrition risk and CA-AKI after PCI. Multivariate logistic regression analysis revealed that malnutrition, as identified by GNRI and PNI, was significantly associated with a higher risk of CA-AKI (moderate-severe malnutrition in GNRI: odds ratio [OR]=1.92, [95% confidence interval (CI), 1.27-2.85]; malnutrition in PNI: OR=1.87, [95% CI, 1.39-2.50]), whereas the CONUT score did not demonstrate a significant difference (P>0.05). Furthermore, GNRI (∆AUC=0.115, P<0.001) and PNI (∆AUC=0.101, P<0.001) exhibited superior predictive ability than the CONUT score for CA-AKI and significantly improved reclassification and discrimination in the fully adjusted model., Conclusions: Malnutrition, especially identified by the GNRI and PNI, was associated with a higher risk of CA-AKI after PCI. GNRI and PNI performed better than the CONUT score in predicting CA-AKI.

Objective: Contrast-induced acute kidney injury (CI-AKI) is a common complication in patients undergoing percutaneous coronary intervention (PCI). Studies have shown that perioperative serum albumin levels may play a role in the occurrence of CI-AKI. In this study, we aimed to investigate the effect of perioperative serum albumin (delta albumin or &Alb) levels on the occurrence and long-term prognosis of CI-AKI patients after PCI., Methods: A total of 959 patients who underwent PCI between January 2017 and January 2019 were selected for this study. A receiver operating characteristic curve was used to determine the optimal cut-off value of the &Alb level for predicting CI-AKI after PCI. Patients were divided into two groups based on the optimal cut-off value: the high &Alb group (&Alb ≥ 4.55 g/L) and the control group (&Alb < 4.55 g/L). The incidences of CI-AKI and major adverse cardiac events (MACEs, including all-cause death, nonfatal myocardial infarction, and target vessel revascularization) were compared between the groups. Cox regression analysis was used to identify predictors of long-term prognosis after PCI., Results: Of the 959 patients, 147 (15.3%) developed CI-AKI after PCI. The CI-AKI group had a greater level of &Alb than did the non-CI-AKI group [(6.14 (3.90-9.10) versus 3.48 (4.31-6.57), P < 0.01)]. The incidence of CI-AKI in the high &Alb group was significantly greater than that in the low group (23.6% versus 8.3%, P < 0.01). After a 1-year follow-up, the incidence of MACEs was significantly greater in the high &Alb group than in the low group (18.6% versus 14.5%, P = 0.030). Cox regression analysis confirmed that CI-AKI was an independent predictor of MACEs at the 1-year follow-up (HR 1.43, 95% CI 1.04-1.96, P = 0.028). In addition, patients with low preoperative serum albumin levels had s significantly greater incidence of MACEs than did those with high preoperative serum albumin levels (23.2% versus 19.5%, P = 0.013)., Conclusion: In summary, high baseline &Alb levels are an independent risk factor for CI-AKI in patients after PCI. The occurrence of CI-AKI in the perioperative period is also an independent predictor of long-term prognosis after PCI. These findings highlight the importance of monitoring &Alb levels and taking steps to prevent CI-AKI in patients undergoing PCI., (© 2024. The Author(s).)

Background and Aims: Contrast-induced nephropathy (CIN), also known as contrast-associated acute kidney injury (CA-AKI) underlies a significant proportion of the morbidity and mortality following coronary angiographic procedures in high-risk patients and remains a significant unmet need. In pre-clinical studies inorganic nitrate, which is chemically reduced in vivo to nitric oxide, is renoprotective but this observation is yet to be translated clinically. In this study, the efficacy of inorganic nitrate in the prevention of CIN in high-risk patients presenting with acute coronary syndromes (ACS) is reported., Methods: NITRATE-CIN is a double-blind, randomized, single-centre, placebo-controlled trial assessing efficacy of inorganic nitrate in CIN prevention in at-risk patients presenting with ACS. Patients were randomized 1:1 to once daily potassium nitrate (12 mmol) or placebo (potassium chloride) capsules for 5 days. The primary endpoint was CIN (KDIGO criteria). Secondary outcomes included kidney function [estimated glomerular filtration rate (eGFR)] at 3 months, rates of procedural myocardial infarction, and major adverse cardiac events (MACE) at 12 months. This study is registered with ClinicalTrials.gov: NCT03627130., Results: Over 3 years, 640 patients were randomized with a median follow-up of 1.0 years, 319 received inorganic nitrate with 321 received placebo. The mean age of trial participants was 71.0 years, with 73.3% male and 75.2% Caucasian; 45.9% had diabetes, 56.0% had chronic kidney disease (eGFR <60 mL/min) and the mean Mehran score of the population was 10. Inorganic nitrate treatment significantly reduced CIN rates (9.1%) vs. placebo (30.5%, P < .001). This difference persisted after adjustment for baseline creatinine and diabetes status (odds ratio 0.21, 95% confidence interval 0.13-0.34). Secondary outcomes were improved with inorganic nitrate, with lower rates of procedural myocardial infarction (2.7% vs. 12.5%, P = .003), improved 3-month renal function (between-group change in eGFR 5.17, 95% CI 2.94-7.39) and reduced 1-year MACE (9.1% vs. 18.1%, P = .001) vs. placebo., Conclusions: In patients at risk of renal injury undergoing coronary angiography for ACS, a short (5 day) course of once-daily inorganic nitrate reduced CIN, improved kidney outcomes at 3 months, and MACE events at 1 year compared to placebo., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Introduction: Contrast-induced nephropathy (CIN) is a common complication after percutaneous coronary intervention (PCI). There is conflicting evidence regarding efficacy of nicorandil in CIN prevention. With respect to ranolazine, there is physiological possibility as well as data in animal study regarding its protective effect against CIN; there is, however, no human data till date., Aim and Objectives: To assess the efficacy of nicorandil and ranolazine in preventing CIN. The secondary endpoint was to measure difference in postprocedure acute kidney injury (AKI) incidence across groups. Also, patients were followed up till 6 months for major adverse events., Material and Methods: This single-center randomized controlled study included 315 patients of coronary artery disease with mild-to-moderate renal dysfunction undergoing elective PCI. Eligible patients were assigned to either nicorandil (n = 105), ranolazine (n = 105) or control group (n = 105) in 1 : 1 : 1 ratio by block randomization. All enrolled patients were given intravenous sodium chloride at rate of 1.0 mL/kg/h (0.5 mL/kg/h for patients with left ventricular ejection fraction <45%) from 6 h before procedure till 12 h after procedure. Iso-osmolar contrast agent (iodixanol) was used for all patients. In addition to hydration, patients in nicorandil group received oral nicorandil (10 mg, 3 times/d) and those in ranolazine group received oral ranolazine (1000 mg, 2 times/d) 1 day before procedure and for 2 days after PCI. Patients in control group received only hydration., Results: Total number of CIN was 34 (10.7%), which included 19 (18.1%) in control, 8 (7.6%) in nicorandil and 7 (6.6%) in ranolazine group. There was significant association of CIN reduction across groups ( P  = 0.012). On pairwise comparison also, there was significant benefit across control and ranolazine as well as control and nicorandil ( P  < 0.025). There was numerically higher incidence of AKI in controls; the difference, however, did not reach statistical significance after applying Bonferroni correction ( P  = 0.044). Over 6-month follow-up, adverse events were similar across groups., Conclusion: While this study adds to existing literature that supports role for nicorandil in CIN prevention, the efficacy of ranolazine in protecting against CIN has been demonstrated in humans for the first time., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Ultra-low contrast administration during coronary angiography has been previously shown to be feasible and safe among patients with stable chronic kidney disease. In the present study, we investigate the safety of ultra-low contrast coronary angiography in patients with pre-existing acute kidney injury (AKI)., Methods: The study was a retrospective single-center evaluation of hospitalized patients who had AKI and required coronary angiography. Ultra-low contrast use was defined as ≤18 mL of contrast media., Results: The cohort consisted of a case series of eight inpatients with AKI who required coronary angiography. The mean age was 57 (±16) years and half were females. All patients had chronic kidney disease with a mean baseline estimated glomerular filtration rate of 34 (±17) mL/min/1.73 m 2 . The mean creatinine before angiography was 3 (±1) mg/dL and volume of contrast administered was 14 (±4) mL. One patient had a 0.1 mg/dL increase in creatinine during admission, and no patients had further AKI up to 1-week postprocedure., Conclusions: The current data suggest that ultra-low contrast coronary angiography can be safely performed in patients with pre-existing AKI The study should be viewed as hypothesis-generating due to its small sample size. A larger cohort is required to validate the results., (© 2024 The Authors. Clinical Cardiology published by Wiley Periodicals, LLC.)

Background: Recent studies have challenged the reported causal association between acute kidney injury and iodinated contrast administration, ascribing some cases to changes in renal function that are independent of contrast administration., Methods: We studied 1779 consecutive patients undergoing right heart catheterization (RHC) at a Veterans Administration Medical Center. We compared the incidence of acute kidney injury and of nephropathy at 3 months in veterans undergoing right and left heart catheterization and coronary angiography (R&LHC) to the incidence of acute kidney injury and of nephropathy at 3 months in patients undergoing RHC only., Results: The incidence of acute kidney injury at 3 days was 47 (9.7%) in the R&LHC group and 58 (9.6%) in the RHC group (P = .99). The incidence of nephropathy at 3 months was 115 (17%) in the L&RHC group and 141 (19.2%) in the RHC group (P = 0.31). In a propensity score-paired analysis of 782 patients and after adjustment for baseline characteristics, the odds ratio for acute kidney injury at 3 days among patients undergoing R&LHC was 1.25 (95% confidence interval, 0.65-2.42; P = .50), and the odds ratio for nephropathy at 3 months was 0.69 (95% confidence interval, 0.46-1.04; P = .08)., Conclusion: The incidence of changes in creatinine consistent with acute kidney injury at 3 days and of nephropathy at 3 months was not significantly different in patients undergoing R&LHC compared with patients undergoing RHC only. This supports the thesis that not all changes in creatinine after procedures involving administration of contrast are caused by the contrast., (Published by Elsevier Inc.)

Older patients (≥75 years) after coronary angiography constitute an increasing proportion, but only limited data are available regarding the prognosis of geriatric contrast-associated acute kidney injury (CA-AKI). Patients (≥75 years) undergoing coronary angiography between December 2010 and September 2013 were consecutively enrolled. CA-AKI was defined as an increase in serum creatinine of 25% or .5 mg/dL from the baseline within 48-72 h of contrast exposure. All-cause mortality was assessed during median 7.5 years (interquartile range [IQR] 6.7-8.7 years) follow-up period. In total, 571 patients aged >75 years undergoing coronary angiography were enrolled in a single center study; 82 (14.4%) patients had CA-AKI. The all-cause mortality during the median 7.5 years follow-up period was 22.0% in patients with CA-AKI and 13.1% in patients without CA-AKI (P = .015). After adjusting for potential confounding factors, the multivariable analysis indicated that CA-AKI was related to an increased risk of all-cause mortality during the median 7.5-year follow-up (hazard ratio [HR]: 2.46; 95% CI: 1.29-4.7; P = .006). CA-AKI is a significant and independent predictor of long-term mortality for patients aged over 75 years who underwent coronary angiography., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.