Prevention Of Contrast-induced Acute Kidney Injury Research Articles

Layer-by-Layer Assembly of Renal-Targeted Polymeric Nanoparticles for Robust Arginase-2 Knockdown and Contrast-Induced Acute Kidney Injury Prevention.

The mitochondrial enzyme arginase-2 (Arg-2) is implicated in the pathophysiology of contrast-induced acute kidney injury (CI-AKI). Therefore, Arg-2 represents a candid target for CI-AKI prevention. Here, layer-by-layer (LbL) assembled renal-targeting polymeric nanoparticles are developed to efficiently deliver small interfering RNA (siRNA), knockdown Arg-2 expression in renal tubules, and prevention of CI-AKI is evaluated. First, near-infrared dye-loaded poly(lactic-co-glycolic acid) (PLGA) anionic cores are electrostatically coated with cationic chitosan (CS) to facilitate the adsorption and stabilization of Arg-2 siRNA. Next, nanoparticles are coated with anionic hyaluronan (HA) to provide protection against siRNA leakage and shielding against early clearance. Sequential electrostatic layering of CS and HA improves loading capacity of Arg-2 siRNA and yields LbL-assembled nanoparticles. Renal targeting and accumulation is enhanced by modifying the outermost layer of HA with a kidney targeting peptide (HA-KTP). The resultant kidney-targeting and siRNA loaded nanoparticles (PLGA/CS/HA-KTP siRNA) exhibit proprietary accumulation in kidneys and proximal tubular cells at 24 h post-tail vein injection. In iohexol-induced in vitro and in vivo CI-AKI models, PLGA/CS/HA-KTP siRNA delivery alleviates oxidative and nitrification stress, and rescues mitochondrial dysfunction while reducing apoptosis, thereby demonstrating a robust and satisfactory therapeutic effect. Thus, PLGA/CS/HA-KTP siRNA nanoparticles offer a promising candidate therapy to protect against CI-AKI.

Neutrophil Extracellular Traps Aggravate Contrast-Induced Acute Kidney Injury by Damaging Glomeruli and Peritubular Capillaries.

Contrast-induced acute kidney injury (CI-AKI) is considered to be the third leading cause of hospital-acquired kidney injury. Current studies mostly suggest that contrast agents mainly harm renal tubular epithelial cells, but we hypothesized that the development of CI-AKI should be the result of the interaction of renal vascular and tubular injury. First we constructed a CI-AKI mouse model and verified the success of the model by pathological injury and serum creatinine level. Immunohistochemistry, protein quantification and qRT-PCR were used to detect the location and level of expression of neutrophil extracellular traps (NETs) in the kidney. Then, we blocked the in vivo accumulation of NETs using GSK484 and DNase I and detected the expression of NETs and the damage of glomerular and peritubular capillaries. We first identified the presence of NETs in CI-AKI mice, and NETs were mainly accumulated in glomeruli and peritubular capillaries. The expression of NETs was positively correlated with the severity of CI-AKI kidney. After inhibition of NETs release or promotion of NETs degradation by drugs, renal vascular endothelial cell injury was reduced and renal pathological changes and creatinine levels were reversed in CI-AKI mice. In addition, inhibition of NETs reduced apoptosis and pyroptosis of renal cells and attenuated inflammation in vivo. These findings suggest that NETs are involved in the development of CI-AKI by damaging glomerular and peritubular capillary endothelial cells. This study will provide a new strategy for clinical prevention and treatment of CI-AKI.

The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.

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

Research progress on animal models of contrast-induced acute kidney injury.

Contrast-induced acute kidney injury (CI-AKI) refers to acute kidney injury that occurs after intravascular contrast media is applied. It is the third most common cause for acute renal failure in hospitalized patients and can cause severe renal impairment and adverse cardiovascular outcomes. In severe cases, it can even lead to the death of the patient. Due to its complicated pathogenesis, the pathogenesis of CI-AKI has not yet been elucidated. Therefore, it is of great significance to further study the pathogenesis for the prevention of CI-AKI. Moreover, a good animal model of CI-AKI is an important tool for in-depth research on the pathogenesis of acute kidney injury induced by contrast agents.

Apelin-13 alleviates contrast-induced acute kidney injury by inhibiting endoplasmic reticulum stress

Contrast-induced acute kidney injury (CI-AKI) is a severe complication associated with significant morbidity and mortality, and effective therapeutic strategies are still lacking. Apelin is an endogenous physiological regulator with antioxidative, anti-inflammatory and antiapoptotic properties. However, the role of apelin-13 in CI-AKI remains unclear. In our study, we found that the protein expression levels of apelin were significantly downregulated in rat kidney tissues and HK-2 cells during contrast media treatment. Moreover, we explored the protective effect of apelin-13 on renal tubule damage using in vitro and in vivo models of CI-AKI. Exogenous apelin-13 ameliorated endoplasmic reticulum stress, reactive oxygen species and apoptosis protein expression in contrast media-treated cells and rat kidney tissues. Mechanistically, the downregulation of endoplasmic reticulum stress contributed critically to the antiapoptotic effect of apelin-13. Collectively, our findings reveal the inherent mechanisms by which apelin-13 regulates CI-AKI and provide a prospective target for the prevention of CI-AKI.

Association of periprocedural phentolamine infusion with favorable outcome in patients with chronic kidney disease and chronic coronary syndrome undergoing coronary catheterization: a prospective randomized controlled pilot study

BackgroundChronic kidney disease (CKD) is a major risk factor for contrast induced acute kidney injury (CI-AKI) in chronic coronary syndrome (CCS) patients undergoing coronary catheterization. We aimed to evaluate the efficacy of phentolamine in prevention of CI-AKI in CKD and CCS patients undergoing percutaneous coronary catheterization for diagnostic angiography ± stenting.MethodsParticipants with CKD and CCS planned for percutaneous coronary catheterization were included, while participants with normal kidney functions were excluded. A consecutive sample of 107 participants (mean age 58.62 ± 8.96 years, 64.5% males) was selected, underwent diagnostic coronary angiography or percutaneous coronary intervention, and received either conventional CI-AKI prevention strategy (group 1) or periprocedural phentolamine and conventional CI-AKI prevention strategy (group 2).ResultsThe percentages of study participants who had CI-AKI were 82.9% for group 1 and 17.1% for group 2, respectively. The incidence rate of CI-AKI was significantly lower in group 2 versus group 1 (p < 0.001). The urine output (ml/kg) and the urine output (ml/hour) within 72 hours post procedure was significantly higher in group 2 versus group 1 (t(105) = − 0.69, p < 0.001, t(105) = − 52.46, p < 0.001, respectively), the peak change in serum creatinine and the percentage of change relative to the baseline serum creatinine at 72 hours post procedure was significantly lower in group 2 versus group 1 (t(102) = 0.2, p 0.018, t(102) = 23.54, p < 0.001, respectively), and the incidence rate of major adverse cardiac and cerebrovascular events within 90 days post procedure was significantly lower in group 2 versus group 1 (t(102) = 1.168, P < 0.001), respectively. There was a statistically significant association of periprocedural phentolamine infusion with prevention of CI-AKI (OR = 0.041, 95% CI 0.0149–0.1128, P < 0.0001).ConclusionOur study highlights the potential role of phentolamine for protection of the kidney in CKD patients planned for coronary catheterization.Trial registrationPan African Clinical Trial Registry Number: PACTR202209493847741.Date of Trial Registration: 22/09/2022.

Contrast-induced acute kidney injury and its contemporary prevention.

The complexity and application range of interventional and diagnostic procedures using contrast media (CM) have recently increased. This allows more patients to undergo procedures that involve CM administration. However, the intrinsic CM toxicity leads to the risk of contrast-induced acute kidney injury (CI-AKI). At present, effective therapy of CI-AKI is rather limited. Effective prevention of CI-AKI therefore becomes crucially important. This review presents an in-depth discussion of CI-AKI incidence, pathogenesis, risk prediction, current preventive strategies, and novel treatment possibilities. The review also discusses the difference between CI-AKI incidence following intraarterial and intravenous CM administration. Factors contributing to the development of CI-AKI are considered in conjunction with the mechanism of acute kidney damage. The need for ultimate risk estimation and the prediction of CI-AKI is stressed. Possibilities of CI-AKI prevention is evaluated within the spectrum of existing preventive measures aimed at reducing kidney injury. In particular, the review discusses intravenous hydration regimes and pre-treatment with statins and N-acetylcysteine. The review further focuses on emerging alternative imaging technologies, alternative intravascular diagnostic and interventional procedures, and new methods for intravenous hydration guidance; it discusses the applicability of those techniques in complex procedures and their feasibility in current practise. We put emphasis on contemporary interventional cardiology imaging methods, with a brief discussion of CI-AKI in non-vascular and non-cardiologic imaging and interventional studies.

Intravenous contrast induced acute kidney injury prevention with high doses of statins

Aim. The aim of our study was to assess the frequency of contrast-induced acute kidney injury (CI-AKI) in patients undergoing computed tomography (CT) with intravenous contrast media and to evaluate the effects of statins in the prevention of CI-AKI. Materials and methods. 181 patients undergoing CT with intravenous contrast media administration were included in prospective observational study (ClinicalTrials.gov ID NCT04666389). The primary endpoint was CI-AKI according to KDIGO criteria (the 25 % rise (or 0,5 mg/dl) of serum creatinine from baseline assessed 48–72 hours after administration of contrast media). There were 120 patients in the group with high dose of statins administration and 60 patients without statin treatment. The most frequent cardiovascular disease was hypertension in both groups — 93 % and 85 % respectively. Results. CI-AKI was diagnosed in 12 (6,7 %) patients — 9 patients in the no statins group and 3 patients in the statins group. The high dose statin administration statistically significant had less frequency of CI-AKI (p = 0,003) compare with no statins group (OR = 0,144, 95 %CI: 0,037–0,554). Conclusion. Statin pretreatment is effective at preventing CI-AKI and should be considered in high-risk patients.

Ultra-low CONtraSt PCI vs conVEntional PCI in patients of ACS with increased risk of CI-AKI (CONSaVE-AKI)

ObjectivesThis prospective, randomized study assessed short-term outcomes and safety of ultra-low contrast percutaneous coronary intervention(ULC-PCI) vs conventional PCI in high risk for contrast induced acute kidney injury(CI-AKI) patients presenting with acute coronary syndrome(ACS). BackgroundPatients at an increased risk of developing CI-AKI can be identified prior to PCI based on their pre-procedural risk scores. ULC-PCI is a novel contrast conservation strategy in such high risk patients for prevention of CI-AKI. Methods82 patients undergoing PCI for ACS were enrolled having estimated glomerular filtration rate(eGFR) < 60 ml/min/1.73 m2 and moderate to very high pre-procedural risk of developing CI-AKI as calculated by Maioli risk calculator. They were randomized into two groups of 41 patients each of ULC-PCI (contrast volume ≤ patient's eGFR) and conventional PCI (contrast volume ≤ 3xpatient's eGFR). Primary end point was development of CI-AKI. ResultsBaseline clinical and angiographic characteristics were similar between groups. Primary outcome of CI-AKI occurred more in patients of the conventional PCI group [7 (17.1%)] than in the ULC PCI group [(0 patients), p = 0.012]. Contrast volume (41.02 (±9.8) ml vs 112.54 (±25.18) ml; P < 0.0001) was markedly lower in the ULC-PCI group. No significant difference in secondary safety outcomes between two study arms at 30 days. IVUS was used in 17% patients in ULC PCI. ConclusionULC-PCI in patients with increased risk of developing CI-AKI is feasible, appears safe, and has the potential to decrease the incidence of CI-AKI specially in resource limited setting such as ours where coronary imaging by IVUS is not possible in every patient.

Meta-analytic Techniques to Assess the Association Between N-acetylcysteine and Acute Kidney Injury After Contrast Administration

The most suitable analytic method to systematically analyze numerous trials with contradictory results is unclear. Multiple trials assessing the use of N-acetylcysteine (NAC) for prevention of contrast-induced acute kidney injury (CI-AKI) have had contradictory results with recent trials confirming a lack of benefit. To systematically review the literature on NAC for the prevention of CI-AKI, and to explore the heterogeneity, publication bias, and small-study effect to determine the most suitable analytic method in a setting where the literature is contradictory. Medline, Embase, and Cochrane Central Register of Controlled Trials databases were used to find randomized clinical trials (RCTs) comparing NAC with any other prophylactic agent or placebo in adults. The search included studies published in English from database inception to January 2020. Two independent reviewers screened the studies, extracted data, and performed the risk of bias assessment. A meta-analysis was conducted about the effect of NAC on CI-AKI, the need for dialysis, and mortality. Fixed and random effects analyses were also performed. Funnel plots and the trim and fill method were used for assessment of publication bias. Metaregression was performed to explore the heterogeneity and subgroup analysis to examine the association between NAC and CI-AKI when studies were categorized according to sample size and number of events. A total of 101 trials were included in this meta-analysis. The median sample size was 112 (range, 20 to 4993). Twenty-nine trials had a sample size of 200 or more, and only 3 trials had a sample size of 500 or more. Forty-five trials reported the need for kidney replacement therapy, and 41 trials reported mortality as an outcome. NAC seemed to show a benefit, with a pooled OR of 0.72 (95% CI, 0.63-0.82) using random effects model and a pooled OR of 0.82 (95% CI 0.76-0.90) using a fixed effects model. However, there was significant heterogeneity (I2 = 37.6; P < .001) and significant publication bias, which was reduced only when restricting to large RCTs (N ≥ 500). The clinical outcomes (ie, the need for kidney replacement therapy and mortality) revealed little heterogeneity and no publication bias, and each provided a robust neutral summary result. In this meta-analysis, NAC was associated with a benefit in the prevention of CI-AKI. However, because of substantial publication bias and other biases, standard meta-analytic techniques resulted in significant heterogeneity and a spurious, or factitious, association, even when using a random effects model. When the analysis was restricted to RCTs with a large sample size to account for publication bias or restricted to trials with clinical outcomes, this issue was reduced and resulted in more robust and neutral effect sizes.

Abstract 13780: Aggressive Hydration and Contrast-Induced Acute Kidney Injury Following Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction: A Randomized Controlled Study

Objective: To evaluate the efficacy of aggressive hydration compared with general hydration for contrast induced acute kidney injury (CI-AKI) prevention among patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). Methods: The ATTEMPT study is an open-label, randomized controlled study at 15 teaching hospitals in China. A total of 560 adult patients were randomly assigned (1:1) to receive aggressive hydration or general hydration treatment. Aggressive hydration group received preprocedural loading dose of 125/250 mL normal saline within 30 minutes, followed by postprocedural hydration performed for 4 hours under left ventricular end-diastolic pressure guidance and additional hydration until 24 hours after pPCI. General hydration group received ≤500 mL 0.9% saline at 1 mL/kg/h for 6 hours after randomization. The primary endpoint is CI-AKI, defined as a &gt;25% or 0.5 mg/dL increased in serum creatinine from baseline during the first 48-72 hours after primary angioplasty. The safety endpoint is hydration relative acute heart failure. Results: From July 2014 and May 2018, 469 patients were enrolled in the final analysis. CI-AKI occurred less frequently in aggressive hydration group than in general hydration group (21.8% vs. 31.1%; RR 0.78, 95% CI 0.61 to 0.98). Hydration relative acute heart failure did not significantly differ between the aggressive hydration group and the general hydration group (7.9% vs. 6.9%, RR 1.07, 95% CI 0.77 to 1.48). Several subgroup analysis showed the better effect of aggressive hydration in CI-AKI prevention in male, renal insufficient and non-anterior myocardial infarction participants. Conclusions: Comparing with general hydration, the peri-operative aggressive hydration seems to be safe and effective in preventing CI-AKI among patients with STEMI undergoing pPCI.

Hydration for prevention of kidney injury after primary coronary intervention for acute myocardial infarction: a randomised clinical trial

ObjectiveTo evaluate the efficacy of aggressive hydration compared with general hydration for contrast-induced acute kidney injury (CI-AKI) prevention among patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention...

POS-039 N-Acetylcysteine and Contrast-induced Acute Kidney Injury: A Systematic Review and Meta-analysis exploring the Heterogeneity, Publication Bias and Small Study effects

Contrast induced acute kidney injury (CI-AKI) is a considerable cause of adverse clinical outcomes and prolonged hospitalisation in patients receiving contrast media for diagnostic and therapeutic procedures. N-acetylcysteine (NAC) has been used for the prevention of CI-AKI and has been evaluated in numerous clinical trials, with contradictory results. Though the final definitive trials demonstrate no efficacy or benefit, previous trials and meta-analysis have quite often reported a benefit. The purpose of this systematic review was to explore the heterogeneity, publication bias, small study effect and determine the most suitable analytic method in this setting with contradictory literature.

Sodium Bicarbonate versus Statins to Prevent Contrast-induced Acute Kidney Injury: A Comprehensive Review

Iodinated contrast agents are commonly used in diagnostic radiography techniques along with therapeutic interventions. Contrast-Induced Acute Kidney Injury (CI-AKI) is a significant problem of all angiographic procedures, triggered by the use of Iodinated Contrast Media (ICM). There are conflicting data concerning the prevention and treatment of CI-AKI. Numerous approaches have been studied to prevent CI-AKI, but the therapy of choice remains undetermined. The cornerstones of CI-AKI prevention include low-osmolar ICM and intravenous hydration. The recommended hydration must be achieved by means of an isotonic solution of saline. Statins were tested against AKI due to their anti-inflammatory action and antioxidant effect on endothelial function. Novel approaches are required to investigate the short-term effects of high dosage atorvastatin versus sodium bicarbonate on CI-AKI prevention. The objective of this review is to compare the findings of various studies that had applied different doses of statins, sodium bicarbonate, and other agents for preventing CI-AKI.

Remote Ischemic Preconditioning for Prevention of Contrast-Induced Acute Kidney Injury in Patients of CKD Stage III and IV Undergoing Elective Coronary Angiography: A Randomized Controlled Trial.

Introduction:Contrast-induced acute kidney injury (CI-AKI) is a serious complication of coronary angiography (CA). The aim of this randomized, parallel group, single blind, sham-controlled trial was to assess the safety and efficacy of the remote ischemic preconditioning on the prevention of CI-AKI.Methods:Patients of 18–80 years of age with CKD 3 and 4, who were admitted for elective coronary angiography in a tertiary care hospital in eastern India were randomized in a 1:1 ratio to standard care with ischemic preconditioning (n = 45; intermittent arm ischemia through 4 cycles of 5-min inflation and 5-min deflation of a blood pressure cuff) or with standard care and sham ischemic preconditioning (n = 42). Overall, both study groups were at moderate risk of developing CI-AKI according to the Mehran risk score. The primary endpoint was the incidence of CI-AKI, defined as an increase in serum creatinine ≥25% or ≥0.5 mg/dL above baseline at 48 h after contrast medium exposure.Results:CI-AKI occurred in 8 patients (19.04%) in the control group and 2 (4.4%) in the remote ischemic preconditioning group (odds ratio, 0.198, 95% confidence interval, 0.087 to 0.452; P = 0.04). No major adverse events were related to remote ischemic preconditioning.Conclusions:This study indicates that remote ischemic preconditioning is a simple and well-tolerated procedure, which reduces the incidence of CI-AKI in CKD 3 and 4 patients undergoing coronary angiography.

Clinical efficacy of Danhong injection in preventing contrast-induced acute kidney injury based on propensity score matching method.

Contrast-induced acute kidney injury (CI-AKI) is the third cause of hospital-acquired AKI, and existing clinical prevention and treatment measures such as hydration therapy and/or administration of antioxidants N-acetylcysteine treatment and other treatments still show little effect on the prevention and treatment of CI-AKI. This study aims to explore the effect of Danhong injection on prevention of CI-AKI. A total of 12 867 patients, who received coronary angiography, percutaneous coronary intervention, enhanced CT or vascular intervention in a tertiary hospital, were enrolled for this study. Among them, 423 in the treatment group received intravenous drip of Danhong injection, and 12 444 in the control group received routine medicine. Propensity score matching was conducted to balance confounding factors between the 2 groups and then the prevention effect of Danhong injection on CI-AKI was compared between them. A total of 423 pairs of patients were matched successfully. The incidence of CI-AKI in the non-Danhong control group was higher than that in the Danhong treatment group (5.7% vs 2.4%). The difference between the 2 groups was statistically significant (P<0.05). CI-AKI occurred maily in the Stage 1 in both the non-Danhong control group and the Danhong treatment group. The number of patients with Stage 1 of AKI in the control group was more than that in the treatment group, and the difference was statistically significant (P<0.05). The incidence of AKI in Stage 2 and Stage 3 was less in both groups, and the difference was not statistically significant (P>0.05). The results of this study support the use of Danhong injection in the prevention of the Stage 1 of CI-AKI.

Едаравон у профілактиці контраст-індукованого гострого ураження нирок

Мета роботи – оцінити ефективність едаравону в запобіганні розвитку контраст-індукованого гострого ураження нирок (КІГУН).Матеріали і методи. Проведено багатоцентрове відкрите проспективне рандомізоване контрольоване дослідження для оцінювання ефективності едаравону в профілактиці КІГУН у пацієнтів із хронічною хворобою нирок (ХХН) 3b–4 стадії. Було сформовано дві групи хворих віком 46–68 років (у середньому (55±3) роки) – основну і контрольну. Основну групу становили 16 пацієнтів з ХХН 3b або 4 стадії (розрахункова швидкість клубочкової фільтрації за формулою СКD-EPI (32±4) мл/хв), які отримували едаравон у дозі 30 мг шляхом внутрішньовенного інфузійного введення. До контрольної групи увійшло 20 пацієнтів із ХХН 3b або 4 стадії (розрахункова швидкість клубочкової фільтрації (33±3) мл/хв), у яких едаравон при проведенні коронароангіографії не застосовували. Пацієнти обох груп перед коронароангіографією отримували внутрішньовенну гідратацію 0,9 % натрію. Первинна кінцева точка: розвиток КІГУН протягом 48 год після введення контрастного засобу та необхідність проведення ниркової замісної терапії. Вторинна кінцева точка: рівень калію в сироватці крові понад 5,5 ммоль/л. Результати та обговорення. Розвиток КIГУН документовано у 4 пацієнтів основної групи та 12 пацієнтів контрольної групи (р≤0,05; RR 0,417; RRR 0,583; RD 0,350; NNT 2,857). Виявлено статистично значущу різницю між групами для обох кінцевих точок, що свідчить про перспективні можливості застосування едаравону для профілактики КІГУН у пацієнтів з ХХН 3b–4 стадії. Аналіз індивідуальних даних показує, що едаравон був ефективнішим у хворих із ХХН 3b стадії (три випадки КІГУН з 10) порівняно з ХХН 4 стадії (один із 2).Висновки. Едаравон може бути перспективним рішенням для профілактики КІГУН у пацієнтів із ХХН 3b–4 стадії, яким терміново виконують коронароангіографію.&#x0D;

SAT-026 THE PROTECTIVE ROLE OF ROSUVASTATIN AGAINST CONTRAST INDUCED ACUTE KIDNEY INJURY; A RANDOMIZED CLINICAL TRIAL

The risk of contrast-induced acute kidney injury (CI-AKI) as a deteriorating factor of renal function has been well demonstrated previously. While the exact mechanism of CI-AKI in not still understood, but many studies have investigated the effect of various drugs in order to prevention of nephrotoxic mechanisms. One of the drugs' category of recent interest is Statins and especially Atorvastatin. The aim of this study was to evaluate the effect of Rosuvastatin – as a newer member of the statins family – in the prevention of CI-AKI. Patients who were candidate for CT scan with contrast during 2018 to 2019 were randomly divided into two groups. The first group received 20 mg Rosuvastatin 24 hours before receiving the contrast followed by 10 mg Rosuvastatin for two consequent days, while the second group received placebo at the same times. Considering the baseline serum's creatinine, patients were examined for probable onset of CI-AKI for next 72 hours after contrast injection. Gathered data were analyzed using SPSS software version 24 and p-value less than 0.05 was considered significant. There were no significant differences regarding age, sex, diabetes mellitus, hypertension and estimated glomerular filtration rate (eGFR) between Rosuvastatin-received group (204 individuals) and placebo-received group (198 patients) at the onset of study. Although there was a decrease in eGFR in the placebo-received group (p-value:0.02), no similar changes were observed in the Rosuvastatin-received group (p-value:0.20) in three days follow up after receiving contrast for CT scan. CI-AKI occurrence were 1% and 4% in Rosuvastatin-received group and placebo-received group respectively and there was a significant difference between groups (p-value:0.04). Based upon our data and similar previous studies, It's believed that Rosuvastatin could be considered as a protective agent against CI-AKI and can reduce renal injuries and decreased eGFR related to contrast injection.

DyeVert™ PLUS EZ System for Preventing Contrast-Induced Acute Kidney Injury in Patients Undergoing Diagnostic Coronary Angiography and/or Percutaneous Coronary Intervention: A UK-Based Cost-Utility Analysis.

BackgroundContrast-induced acute kidney injury (CI-AKI) is a complication commonly associated with invasive angiographic procedures and is considered the leading cause of hospital-acquired acute kidney injury. CI-AKI can lead to a prolonged hospital stay, with a substantial economic impact, and increased mortality. The DyeVert™ PLUS EZ system (FDA approved and CE marked) is a device that has been developed to divert a portion of the theoretical injected contrast media volume (CMV), reducing the overall volume of contrast media injected and aortic reflux, and potentially improving long-term health outcomes.ObjectivesTo assess the long-term costs and health outcomes associated with the introduction of the DyeVert™ PLUS EZ system into the UK health care service for the prevention of CI-AKI in a cohort of patients with chronic kidney disease (CKD) stage 3–4 undergoing diagnostic coronary angiography (DAG) and/or percutaneous coronary intervention (PCI), and to compare these costs and outcomes with those of the current practice.MethodsA de novo economic model was developed based on the current pathway of managing patients undergoing DAG and/or PCI and on evidence related to the clinical effectiveness of DyeVert™ in terms of its impact on relevant clinical outcomes and health service resource use. Clinical data used to populate the model were derived from the literature or were based on assumptions informed by expert clinical input. Costs included in the model were from the NHS and personal social services perspective and obtained from the literature and UK-based routine sources. Probabilistic distributions were assigned to the majority of model parameters so that a probabilistic analysis could be undertaken, while deterministic sensitivity analyses were also carried out to explore the impact of key parameter variation on the model results.ResultsBase-case results indicate that the intervention leads to cost savings (− £435) and improved effectiveness (+ 0.028 QALYs) over the patient’s lifetime compared with current practice. Output from the probabilistic analysis points to a high likelihood of the intervention being cost-effective across presented willingness-to-pay (WTP) thresholds. The overall long-term cost saving for the NHS associated with the introduction of the DyeVert™ PLUS EZ system is over £19.7 million for each annual cohort of patients. The cost savings are mainly driven by a lower risk of subsequent diseases and their associated costs.ConclusionsThe introduction of the DyeVert™ PLUS EZ system has the potential to reduce costs for the health care service and yield improved clinical outcomes for patients with CKD stage 3–4 undergoing angiographic procedures.Electronic supplementary materialThe online version of this article (10.1007/s41669-020-00195-x) contains supplementary material, which is available to authorized users.

Contrast induced acute kidney injury in interventional cardiology: an update and key guidance for clinicians.

Contrast-induced acute kidney injury (CI-AKI) is a serious complication that can affect outcome and prognosis of patients undergoing percutaneous diagnostic and interventional procedures in catheterization laboratories. There have been advancements in case definition and epidemiology. Additionally strategies have emerged that are positioned to have impact in the catheterization laboratory for patients undergoing cardiovascular procedures. The aim of this review is to provide the state-of-the-art of diagnosis, prevention and management of CI-AKI in interventional cardiology.