Contrast-induced Kidney Injury Research Articles

Renal outcomes after contrast exposure in patients with diabetes who use sodium-glucose cotransporter 2 inhibitors.

Contrast-induced nephropathy has become increasingly prevalent as the age and prevalence of comorbidities in the general population have increased. Most cases of contrast-induced nephropathy are reversible; however, some may progress to acute kidney disease, and subsequently, to chronic kidney disease. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are known for their renoprotective effects. However, whether the use of these inhibitors affects the risk of contrast-induced kidney injury remains unclear. Data were collected from the Taipei Medical University Clinical Research Database. We included patients with diabetes who had contrast exposure between 2016 and 2020 because of computed tomography or coronary angiography. The primary outcome was the risk of a major adverse kidney event (MAKE), which encompassed acute kidney disease, chronic kidney disease progression, and the need for renal replacement therapy. Overlap weighting was performed to reduce the effects of potential confounders. This study included 12 421 patients, who were divided into two groups: SGLT2i users (n = 920) and nonusers (n = 11 501). The follow-up period after contrast exposure was 6months. The risk of a MAKE was lower in SGLT2i users than in nonusers (incidence, 36.9 vs. 49.9 per 1000 person-months, respectively; P = .0011). Furthermore, the incidence of acute kidney disease or chronic kidney disease progression was significantly lower in the SGLT2i users than in nonusers. However, no significant between-group difference was noted in the incidence of other MAKEs. SGLT2i may be safely used in diabetic patients needing contrast exposure. The risk of a MAKE may be lower in SGLT2i users than in nonusers.

The renal outcome post contrast exposure in patient with diabetes and SGLT2 inhibitor

Abstract Introduction Contrast-induced nephropathy (CIN) is increasingly prevalent as the increased age and comorbidities. Though most CIN can be reversible, some may progress to acute kidney disease (AKD) and subsequent chronic kidney disease (CKD)1-3. Sodium–glucose cotransporter-2 (2SGLT) inhibitor has been known to bring better renal outcomes 4-7. However, whether it affect contrast-induced kidney injury is not known well. we Purpose We aimed to investigate the renal outcomes post-contrast exposure in patients with diabetes and SGLT2 inhibitor. Materials and methods We used the Taipei Medical University Clinical Research Database (TMUCRD), composed of clinical data from 3 teaching hospitals. which stores electronic health data of 3 million patients. Patients with diabetes and exposure to contrast in CT-imaging studies or catheter-based angiography from 2016 to 2020 were included. The primary outcome was major kidney adverse event (MAKE), which included acute kidney disease (AKD), chronic kidney disease (CKD), renal replacement therapy (RRT), new onset of urinary albumin-creatinine ratio (uACR), eGFR decline ≥ 40% and all-cause mortality. We used overlap weighting to reduce confounding factors, as in observational studies. Results A total of 12,421 patients were included in this study, of them, 920 and 11501 patients were categorized to SGLT2 inhibitor users and non SGLT2 inhibitor users, respectively. SGLT2 inhibitor user had lower MAKE risk as compared with non-SGLT2 inhibitor i user (incidence rate: 37.9 v.s. 53.4 per 1,000 person months, P value = 0.0002) after exposure to contrast media. The incidence rate of AKD, CKD, and eGFR decline ≥ 40% were significantly lower in SGLT2 inhibitor user. However, there were no significantly different in the risk of RRT, new onset of uACR or all-cause mortality. Conclusions In this retrospective cohort study, we found that SGLT2 inhibitor user was associated with lower MAKE comparing with non-SGLT2 inhibitor user after contrast exposure in patients with diabetes.Outcomes of DM patients with PCI or contKaplan-Meier plot of major adverse kidne

Enhanced external counterpulsation, focusing on its effect on kidney function, and utilization in patients with kidney diseases: a systematic review.

Enhanced external counterpulsation (EECP) is provided by a noninvasive device positively affecting cardiovascular function via mechanisms called diastolic augmentation and systolic unloading. The renal aspects of EECP therapy have not been extensively investigated. To assess the effect of EECP on renal function and to determine the application in patients with kidney disease. MEDLINE, EMBASE, SCOPUS, and Cochrane CENTRAL databases were searched for all studies involving EECP treatments. The title and abstract of all searched literatures were screened, and those focusing on renal outcome or conducting in kidney disease patients were selected. Eight studies were included in the qualitative analysis. EECP increases stroke volume, mean arterial pressure, renal artery blood flow, renal plasma flow, glomerular filtration rate (GFR), plasma atrial natriuretic peptide, urine volume, and urinary sodium chloride excretion, but reduces the plasma concentration of renin and endothelin-1 in healthy subjects. A single session of EECP after radioactive contrast exposure could provide increased contrast clearance, and this reduces contrast-induced kidney injury in patients, irrespective of previous kidney function. Thirty-five-hour sessions of EECP treatment were illustrated to increase long-term estimated GFR in patients with chronic angina and heart failure. In cirrhotic patients, EECP fails to improve GFR and renal vascular resistance. EECP device could maintain blood pressure, decrease angina symptoms, and increase cardiac perfusion in hemodialysis patients. EECP treatment potentially increases renal perfusion and prevents kidney injury in several conditions. EECP possibly provides beneficial effects on hemodynamics and cardiac function in hemodialysis patients.

Prognostic Nutritional Index Combined with Triglyceride-Glucose Index to Contrast a Nomogram for Predicting Contrast-Induced Kidney Injury in Type 2 Diabetes Mellitus Patients with Acute Coronary Syndrome After Percutaneous Coronary Intervention.

Our objective was to develop and validate a nomogram model aiming at predicting the risk of contrast-induced acute kidney injury (CI-AKI) following percutaneous coronary intervention (PCI) in patients suffering fromtype 2 diabetes mellitus (T2DM) and also diagnosed with acute coronary syndrome (ACS). The study gathered data from 722 T2DM patients with ACS who received PCI treatment at the Affiliated Hospital of Xuzhou Medical University between February 2019 and December 2022, serving as the training set. Considering the validation set, the study included 217 patients who received PCI at the East Affiliated Hospital of Xuzhou Medical University. The patients were classified into CI-AKI and non-CI-AKI groups. The study employed univariate and multivariate logistic analysis for identifying independent risk factors for CI-AKI, followed by developing a predictive nomogram model for CI-AKI risk using R software. The predictive performance and clinical utility of the nomogram were assessed through internal and external validation, utilizing the areas under the receiver operating characteristic curve (AUC-ROC), the Hosmer-Lemeshow test and calibration correction curve, and decision curve analysis (DCA). The nomogram comprised four variables: age, estimated glomerular filtration rate (eGFR), triglyceride-glucose (TyG) index, and prognostic nutritional index (PNI). The AUC-ROC were 0.785 (95% confidence interval (CI) 0.729-0.841) and 0.802 (95% CI 0.699-0.905) for the training and validation cohorts, respectively, indicating a high discriminative ability of the nomogram. The calibration assessment and decision curve analysis have substantiated the strong concordance and clinical usefulness of the aforementioned. The nomogram exhibits favorable discrimination and accuracy, enabling it to visually and individually identify pre-procedure high-risk patients, and possesses a predictive capacity regarding CI-AKI incidence after PCI in patients diagnosed with both T2DM and ACS.

Abstract Number ‐ 254: Yield of CTA in Patients over 50 with Brain Hemorrhages at Sites Typical for Hypertension

Introduction Approximately 10%–15% of acute strokes are spontaneous, nontraumatic intraparenchymal cerebral hemorrhage (IPH). Hypertension (HTN), amyloid angiopathy, or impaired coagulation cause most spontaneous IPHs, in which case the CTA is unlikely to identify an underlying vascular lesion. Prior investigators have identified clinical and non‐contrast CT (NCCT) features that increase the likelihood of identifying a vascular etiology for an IPH, including younger age (< 40–50), absence of hypertension, and presence of subarachnoid (SAH) or intraventricular hemorrhage (IVH). Findings from earlier studies of patients with IPH suggested that older age, HTN, together with certain locations (basal ganglia, thalamus, cerebellum, and pons) could reliably exclude IPH patients with underlying lesions. We aimed to assess the yield of CTA, a costly study with risks of radiation, contrast induced renal injury and death, in identifying vascular lesions in this group. Methods This retrospective study involved reviewing medical records of all patients admitted to Carilion RMH hospital for brain hemorrhage during the period 2008–2020, inclusive. Patients were considered if they were over 50 year of age, had HTN (and/or left ventricular hypertrophy on electrocardiograms or echocardiograpy) and IPH in the thalamus, basal ganglia, cerebellum or pons. Patients with SAH, lobar IPH, traumatic IPH, pure IVH, and patients with known vascular lesions were excluded. Imaging of all patients was reviewed with attention to finding CTAs showing vascular lesions that might have caused of the recent symptomatic IPH (arteriovenous malformations, aneurysms, venous anomalies and dural venous sinus thrombosis). Small saccular aneurysms at remote sites were not considered relevant, nor were intra‐ or extracranial stenoses. Results A total of (446) charts were reviewed, of which 143 met the inclusion criteria (94 males and 49 females). Family history was positive for cerebral aneurysm in one patient and Alzheimer’s with brain hemorrhage in another. Twenty‐six patients were on anticoagulation: 10 on NOAC, 14 on Warfarin (INR was < 2 in 8, 2–3 in 5, and >3 in only one patient). One was on subcutaneous heparin (PTT was 53). No other patient had major coagulation abnormalities; only 5 patients had platelets count < 100K, the lowest was 62K. CTA was negative for underlying vascular lesion at the site of bleeding in all 143 patients, confidence interval 2.6% using Confidence intervals for proportions, using Wilson’s method for proportions. Conclusions In patients over 50 year of age with evidence of hypertension, and ICH in the basal ganglia, thalamus, brain stem and cerebellum; the diagnostic yield of CTA is negligible. Performing this study routinely in the evaluation of these patient increases health care costs, and exposes patients to the risks of unnecessary radiation, contrast induced kidney injury and death. We recommend against the routine use of CTA in patients meeting the above criteria.

The effect of lycopene on contrast-induced nephrotoxicity in diabetic patients undergoing coronary angiography

Introduction: Radiocontrast nephrotoxicity refers to one of the most prevalent and key complications in diabetic patients. Objectives: This study was aimed to investigate the therapeutic and protective effect of lycopene on contrast-induced nephrotoxicity (CIN) in diabetic patients undergoing coronary angiography. Patients and Methods: In this study, 113 patients who took lycopene with prevention of contrast induced kidney injury regime (lycopene group) or prevention of kidney injury regimen alone (regimen group) were investigated through medical records. Oral lycopene was administered 24 hours before to 72 hours after the angiography. Blood urea nitrogen (BUN), creatinine (Cr), and glomerular filtration rate (GFR) were assessed and recorded in a checklist. SPSS software was conducted for data analysis. Results: At the baseline, there was no significant difference between the mean of urea, Cr, and GFR (P>0.05). However, after administration of lycopene, a significant difference between the mean BUN was observed among groups (P<0.001), with lower rate in the patients taking oral lycopene. Although the mean Cr decreased after the administration of oral lycopene, no statistically significant difference was seen (P = 0.08). The mean GFR was not significant different between the two groups of regimen and lycopene (P=0.44). Conclusion: In patients with diabetes, taking lycopene for CIN may help improve some biochemical factors; nevertheless, its positive effect on the improvement of nephrotoxicity indices cannot be certainly determined.

Neutrophil gelatinase-associated lipocalin monitoring reveals persistent subclinical kidney injury following intraarterial administration of iodinated contrast agents

Clinically overt contrast-induced nephropathy (CIN) is one of the most feared complications in patients exposed to iodinated contrast media and has been extensively studied over the years. Meanwhile, the incidence and evolution of subclinical contrast-induced kidney injury remain elusive. With the continuous increase in the number of patients that are repeatedly exposed to contrast media, elucidating these issues is of critical importance. Accordingly, we aimed to evaluate the incidence and the evolution of clinical and subclinical kidney injury in patients exposed to contrast media. A total of 178 patients who underwent elective percutaneous angioplasty procedures were evaluated prospectively. Serum creatinine and neutrophil gelatinase-associated lipocalin (NGAL) levels were evaluated pre-procedurally, 48 h and 1 month after administration of contrast media. The evolution of creatinine and NGAL levels was analyzed at the three time points, and the potential predictors of contrast-induced clinical and subclinical renal injury were evaluated. Clinically overt CIN occurred in 10 (5.6%) patients. Baseline serum creatinine and the volume of contrast media were the only independent predictors of CIN and in all 10 patients creatinine levels returned to baseline by 1 month (p = 0.32). Subclinical contrast-induced kidney injury was much more common, affecting 32 (17.9%) patients, was only predicted by the baseline serum creatinine, and persisted in 53.1% of patients after 1 month. This study showed that whereas clinically overt CIN is rather rare and regressive, subclinical contrast-induced kidney injury is considerably more frequent, affecting almost 18% of patients that receive intraarterial contrast media. More importantly, subclinical kidney injury persisted after 1 month in more than 50% of the initially affected patients, who may thus be at increased risk for further renal impairment, particularly if exposed to nephrotoxic agents or repeated administration of contrast media.

Three-Dimensional Kidney-on-a-Chip Assessment of Contrast-Induced Kidney Injury: Osmolality and Viscosity.

Increased viscosity of concentrated contrast media (CM) in the renal tubules can perturb renal hemodynamics and have a detrimental effect on tubular epithelial cells. However, the effects of viscosity on contrast-induced nephropathy (CIN) remain poorly understood. Conventional in vitro culture studies do not reflect the rheological properties of CM. Therefore, we investigated the effects of CM viscosity on renal tubules using a kidney-on-a-chip and two different types of CM. Renal proximal tubule epithelial cells (RPTEC) were cultured in a three-dimensional microfluidic culture platform under bidirectional fluid shear stress. We treated the RPTEC with two types of CM: low- (LOCM, iopromide) and iso-osmolar contrast media (IOCM, iodixanol). Renal tubular cell injury induced by LOCM and IOCM was examined under different iodine concentrations (50–250 mgI/mL) and shear-stress conditions. LOCM showed a significant dose-dependent cytotoxic effect, which was significantly higher than that of IOCM under static and low-to-moderate shear stress conditions. However, high shear-stress resulted in reduced cell viability in IOCM; no difference between IOCM and LOCM was found under high shear-stress conditions. The cytotoxic effects were pronounced at a mean shear stress of 1 dyn/cm2 or higher. The high viscosity of IOCM slowed the fluid flow rate and augmented fluid shear-stress. We suggest an alternative in vitro model of CIN using the three-dimensional kidney-on-a-chip. Our results indicate a vital role of viscosity-induced nephrotoxicity under high shear-stress conditions, contrary to the findings of conventional in vitro studies.

Endovascular Thrombectomy for Pediatric Acute Ischemic Stroke

Evidence regarding the utilization and outcomes of endovascular thrombectomy (EVT) for pediatric ischemic stroke is limited, and justification for its use is largely based on extrapolation from clinical benefits observed in adults. Weighted discharge data from the National Inpatient Sample were queried to identify pediatric patients with ischemic stroke (<18 years old) during the period of 2010 to 2019. Complex samples statistical methods were used to characterize the profiles and clinical outcomes of EVT-treated patients. Propensity adjustment was performed to address confounding by indication for EVT based on disparities in baseline characteristics between EVT-treated patients and those medically managed. Among 7365 pediatric patients with ischemic stroke identified, 190 (2.6%) were treated with EVT. Utilization significantly increased in the post-EVT clinical trial era (2016-2019; 1.7% versus 4.0%; P<0.001), while the use of decompressive hemicraniectomy decreased (2.8% versus 0.7%; P<0.001). On unadjusted analysis, 105 (55.3%) EVT-treated patients achieved favorable functional outcomes at discharge (home or to acute rehabilitation), while no periprocedural iatrogenic complications or instances of contrast-induced kidney injury were reported. Following propensity adjustment, EVT-treated patients demonstrated higher absolute but nonsignificant rates of favorable functional outcomes in comparison with medically managed patients (55.3% versus 52.8%; P=0.830; adjusted hazard ratio, 1.01 [95% CI, 0.51-2.03]; P=0.972 for unfavorable outcome). Among patients with baseline National Institutes of Health Stroke Scale score >11 (75th percentile of scores in cohort), EVT-treated patients trended toward higher rates of favorable functional outcomes compared with those treated medically only (71.4% versus 55.6%; P=0.146). In a subcohort assessment of EVT-treated patients, those administered preceding thrombolytic therapy (n=79, 41.6%) trended toward higher rates of favorable functional outcomes (63.3% versus 49.5%; P=0.060). This cross-sectional evaluation of the clinical course and short-term outcomes of pediatric patients with ischemic stroke treated with EVT demonstrates that EVT is likely a safe modality which confers high rates of favorable functional outcomes.

Incidence of Contrast-Induced Nephropathy and Post-Operative Outcomes in Patients Undergoing Chimney Endovascular Aortic Aneurysm Repair.

Chimney endovascular aortic aneurysm repair (ch-EVAR) has become a valid alternative to treat complex aneurysms but the occurrence of contrast-induced kidney injury (CI-AKI) is poorly known. This study investigated the incidence and the impact of CI-AKI on post-operative outcomes after ch-EVAR. Consecutive patients who underwent ch-EVAR between July 2010 and 2021 were retrospectively included. CI-AKI was defined based on plasma creatinine levels within 7days after the intervention according to the "Kidney Disease Improving Global Outcomes" (KDIGO) classification. Among 102 patients included, CI-AKI occurred in 14 cases (13.7%). The 30-day post-operative mortality and complications were significantly higher in patients who developed CI-AKI compared with those who did not (50 vs 9.1%, P = .001 and 57.1 vs 20.5%, P = .007). Over a median follow-up of 24months (3-39), overall mortality was also significantly higher (78.6 vs 33.0%, P = .002). The pre-operative platelet-to-lymphocyte ratio (PLR) was significantly higher in patients who developed CI-AKI (224.5 vs 147.6, P = .008). CI-AKI is frequent after ch-EVAR and is associated with worse post-operative outcomes. This should increase awareness of clinicians to optimize preventive and therapeutic strategies.

POS-076 Serum Cystatin C as early marker for AKI of Patients after Coronary Angiography: a Prospective, Observational Study in Mexican population

Cystatin C is only filtered and metabolized in the kidney, which makes it the ideal marker of kidney function. High sensitivity and specificity for early detection of acute kidney injury and contrast induced kidney injury (C-AKI). Early identification of C-AKI after percutaneous coronary intervention may help to change the prognosis of this patients.

Usefulness of Adding Pre-procedural Glycemia to the Mehran Score to Enhance Its Ability to Predict Contrast-induced Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention Development and Validation of a Predictive Model

The Mehran score is the most widely accepted tool for predicting contrast-induced acute kidney injury (CI-AKI), a major complication of percutaneous coronary intervention (PCI). Similarly, abnormal fasting pre-procedural glycemia (FPG) represents a modifiable risk factor for CI-AKI, but it is not included in current risk models for CI-AKI prediction. We sought to analyze whether adding FPG to the Mehran score improves its ability to predict CI-AKI following PCI. We analyzed 671 consecutive patients undergoing PCI (age 69 [63,75] years, 23% females), regardless of their diabetic status, to derive a revised Mehran score obtained by including FPG in the original Mehran score (Derivation Cohort). The new risk model (GlyMehr) was externally validated in 673 consecutive patients (Validation Cohort) (age 69 [62,76] years, 21% females). In the Derivation Cohort, both FPG and the original Mehran score predicted CI-AKI (AUC 0.703 and 0.673, respectively). The GlyMehr score showed a better predictive ability when compared with the Mehran score both in the Derivation Cohort (AUC 0.749, 95%CI 0.662 to 0.836; p=0.0016) and the Validation Cohort (AUC 0.848, 95%CI, 0.792 to 0.903; p=0.0008). In the overall population (n=1344), the GlyMehr score confirmed its independent and incremental predictive ability regardless of diabetic status (p ≤0.0034) or unstable/stable coronary syndromes (p ≤0.0272). In conclusion, adding FPG to the Mehran score significantly enhances our ability to predict CI-AKI. The GlyMehr score may contribute to improve the clinical management of patients undergoing PCI by identifying those at high risk of CI-AKI and potentially detecting modifiable risk factors.

MO345LIFESAVING BIOMARKERS IN CONTRAST-INDUCED ACUTE KIDNEY INJURY IN ADULT CRITICAL ICU PATIENTS

Abstract Background : - Intravenous administration of radiocontrast media is referred to as contrast-induced kidney injury (CI-AKI).CI-AKI is described as the third most common cause of new AKI in hospitalized patients. The occurrence of CI-AKI is reported up to 55% in these high-risk patients.: NGAL (Neutrophil gelatinase-associated Lipocalin)and Cystatin C have been found an early and sensitive marker of acute kidney injury (AKI). Aims To evaluate biomarkers in plasma (P) and urine (U) after intravenous contrast in adult ICU patients. Method Total of 36 patients recruited as per inclusion criteria. ICU patients who were &amp;gt;18 years with radiographic contrast for diagnostic or interventional computed tomography (CT scan), were included. After ethical approval, samples of 5 ml blood and 5 ml urine were collected before contrast exposure and at 4 h, 24 h, and 48 h after contrast exposure. NGAL and Cystatin C assay was done by ELISA, and urinary levels were normalized as per urine creatinine (UCr) values for each sample. In the present study, CI-AKI is defined as a rise in SCr of ≥0.3 mg/dl within 48 hrs. Data presented in a mean or median analysis performed. Results In this study, 30 CT scan episodes requiring intravenous contrast in 25 ICU patients were included. Median age was 36 yrs and 13 (43%) were male. On day of inclusion, median SOFA score was 3; 16% In patients having CI-AKI, mean values changes from pre-contrast to at 4 h, 24 h and 48 h after contrast are presented..Kinetics of plasma (P) and urine (U) NGAL and Cystatin C levels (Mean±SD) with p value among patients having CI-AKI P NGAL (ng/ml), Before Contrast(BC)( 708.5±201.76) , 04hrC(851.5±332.05, p=0.07), 24hrC(1093.25±225.03, p=0.02), 48hrC(788±323.4, p=0.21), UNGAL (ng/mg of U Cr)BC(67.63±48.09) , 04hrC(39.69±19.79, p=0.07) , 24hrC(101.97±90, p=0.12) , 48hrC(59.87±56.85, p=0.73) , P Cystatin C (ng/ml) BC(4698.85±574.71), 04hrC(4704.57±1144.87) , p=0.02) , 24hrC(4428.85±1135.73, p=0.03), 48hrC(4288.85±435.8, p=0.17), U Cystatin C (ng/mg of UCr) BC(3 46.06±224.7), 04hrC(219.66±72.18, p=0.91), 24hrC (470.21±536.28, p=0.99), 48hrC(633.61±811.77, p=0.23). Conclusion ROC curve analysis during pre-contrast exposure: NGAL, and Cystatin C), both plasma and urine level AUC was significantly higher in patients who develop CI-AKI and Post-contrast exposure Plasma levels AUC significantly higher than Urine levels.

A Simple Nomogram to Predict Contrast-Induced Acute Kidney Injury in Patients with Congestive Heart Failure Undergoing Coronary Angiography.

Background Patients with congestive heart failure (CHF) are vulnerable to contrast-induced kidney injury (CI-AKI), but few prediction models are currently available. Therefore, we aimed to establish a simple nomogram for CI-AKI risk assessment for patients with CHF undergoing coronary angiography. Methods A total of 1876 consecutive patients with CHF (defined as New York Heart Association functional class II-IV or Killip class II-IV) were enrolled and randomly (2:1) assigned to a development cohort and a validation cohort. The endpoint was CI-AKI defined as serum creatinine elevation of ≥0.3 mg/dL or 50% from baseline within the first 48–72 hours following the procedure. Predictors for the simple nomogram were selected by multivariable logistic regression with a stepwise approach. The discriminative power was assessed using the area under the receiver operating characteristic (ROC) curve and was compared with the classic Mehran score in the validation cohort. Calibration was assessed using the Hosmer–Lemeshow test and 1000 bootstrap samples. Results The incidence of CI-AKI was 9.06% (170) in the total sample, 8.64% (n = 109) in the development cohort, and 9.92% (n = 61) in the validation cohort (P=0.367). The simple nomogram including four predictors (age, intra-aortic balloon pump, acute myocardial infarction, and chronic kidney disease) demonstrated a similar predictive power as the Mehran score (area under the curve: 0.80 vs. 0.75, P=0.061), as well as a well-fitted calibration curve. Conclusions The present simple nomogram including four predictors is a simple and reliable tool to identify CHF patients at risk of CI-AKI, whereas further external validations are needed.

Evaluation of coenzyme Q10 combined with or without N-acetyl cysteine or atorvastatin for preventing contrast-induced kidney injury in diabetic rats.

Combined antioxidants effect for prevention of contrast-induced nephropathy (CIN) remains unclear. This study assessed the potential protective effects of coenzyme Q10 (CoQ10) alone or combined with N-acetyl cysteine (NAC) or atorvastatin against CIN in diabetic rats. Animals were randomly divided into five groups, including control and four disease groups with CIN and diabetes. Group 2 included diabetic rats with CIN. Groups 3-5 included diabetic rats that received CoQ10, CoQ10 and NAC, or CoQ10 and atorvastatin, respectively, before CIN induction. Serum, urine, and tissue were collected to evaluate renal protective effects of tested agents. Renal biomarkers, oxidative stress, and histopathological alterations were investigated. Rats with CIN showed significant renal impairment as revealed by the deleterious effects on kidney function and histology. While induction of CIN did not affect the renal levels of catalase, glutathione peroxidase (GPx), and thiobarbituric acid reactive substances, pretreatment of animals with CoQ10/NAC showed significant increase in GPx and catalase levels versus controls. Lastly, pretreatment with CoQ10/atorvastatin showed regenerative effect on distal tubules with mild kidney histology alterations relative to CIN rats. The combined use of CoQ10/atorvastatin could be a potential strategy to prevent CIN. However, future studies are warranted to test different combinations for longer prophylactic periods.

Abstract 14808: Acute Kidney Injury and Adverse Outcomes in Patients Undergoing Right Heart Catheterization versus Patients Undergoing Right and Left Heart Catheterization and Coronary Angiography

Background: Contrast induced nephropathy (CIN), or contrast-induced acute kidney injury is considered a complication of intravascular administration of iodinated contrast material. However, more recent studies have challenged the reported incidence of contrast nephropathy. We compared the incidence of acute kidney injury and of nephropathy at 3 months in patients undergoing only right heart catheterization (RHC) to patients undergoing right and left heart catheterization (R&amp;LHC) and coronary angiography. Methods and Results: We studied 1779 consecutive patients at a Veterans Administration Medical Center, of which 869 underwent only RHC, which does not involve the administration of iodinated contrast media, and 910 patients who underwent R&amp;LHC and coronary angiography. Creatinine values at 72 hours after the respective procedure were available in 938 patients and creatinine values at 3 months were available in 1246 patients. The incidence of acute kidney injury (defined as an increase in serum creatinine of 0.5 mg/dL or 25% compared to baseline) at 3 days was 34 (7.5%) in the RHC group and 46 (9.5%) in the R&amp;LHC group (P=0.31). The incidence of nephropathy at 3 months was 89 (15.6%) in the RHC group and 113 (12.2%) in the R&amp;LHC group (P=0.15). On multivariable analysis including adjustment for a propensity score, CIN at 3 days was not significantly associated with R&amp;LHC (odds ratio (OR) 1.02, 95% confidence interval (CI) 0.98-1.05; P=0.56) and neither was nephropathy at 3 months (OR 1.01, 95% CI 0.98-1.04; P=0.22). Patients undergoing R&amp;LHC had a lower mortality at 12 months (hazard ratio 0.57, 95% CI 0.43-0.77; P&lt;0.001). Conclusions: The incidence of acute kidney injury was not significantly different in patients undergoing RHC compared to patients undergoing R&amp;LHC and coronary angiography, even though the former received no contrast dye. The incidence of nephropathy at 3 months was also not significantly different between the two groups while mortality was significantly lower in the group of patients undergoing R&amp;LHC. This suggests that serum creatinine is a nonspecific diagnostic marker for contrast induced-kidney injury and that long-term outcomes are not associated with the administration of contrast in this population.

Minimal risk of contrast-induced kidney injury in a randomly selected cohort with mildly reduced GFR

ObjectivesPrevious large studies of contrast-induced or post-contrast acute kidney injury (CI-AKI/PC-AKI) have been observational, and mostly retrospective, often with patients undergoing non-enhanced CT as controls. This carries risk of inclusion bias that makes the true incidence of PC-AKI hard to interpret. Our aim was to determine the incidence of PC-AKI in a large, randomly selected cohort, comparing the serum creatinine (Scr) changes after contrast medium exposure with the normal intraindividual fluctuation in Scr.MethodsIn this prospective study of 1009 participants (age 50–65 years, 48% females) in the Swedish CArdioPulmonary bioImage Study (SCAPIS), with estimated glomerular filtration rate (eGFR) ≥ 50 mL/min, all received standard dose intravenous iohexol at coronary CT angiography (CCTA). Two separate pre-CCTA Scr samples and a follow-up sample 2–4 days post-CCTA were obtained. Change in Scr was statistically analyzed and stratification was used in the search of possible risk factors.ResultsMedian increase of Scr post-CCTA was 0–2 μmol/L. PC-AKI was observed in 12/1009 individuals (1.2%) according to the old ESUR criteria (> 25% or > 44 μmol/L Scr increase) and 2 individuals (0.2%) when using the updated ESUR criteria (≥ 50% or ≥ 27 μmol/L Scr increase). Possible risk factors (e.g., diabetes, age, eGFR, NSAID use) did not show increased risk of developing PC-AKI. The mean effect of contrast media on Scr did not exceed the intraindividual Scr fluctuation.ConclusionsIohexol administration to a randomly selected cohort with mildly reduced eGFR is safe, and PC-AKI is very rare, occurring in only 0.2% when applying the updated ESUR criteria.Key Points• Iohexol administration to a randomly selected cohort, 50–65 years old with mildly reduced eGFR, is safe and PC-AKI is very rare.• Applying the updated ESUR PC-AKI criteria resulted in fewer cases, 0.2% compared to 1.2% using the old ESUR criteria in this cohort with predominantly mild reduction of renal function.• The mean effect of CM on Scr did not exceed the intraindividual background fluctuation of Scr, regardless of potential risk factors, such as diabetes or NSAID use in our cohort of 1009 individuals.

Contrast-induced acute kidney injury in chronic coronary artery disease patients with diabetes mellitus and obesity

To assess the influence of diabetes mellitus and obesity on contrast-induced acute kidney injury risk in patients with chronic coronary artery disease requiring percutaneous coronary intervention. 1023 patients with chronic coronary artery disease were enrolled in a prospective, open, cohort study (ClinicalTrials.gov ID NCT04014153). Contrast-induced acute kidney injury was defined as an increase of 25% or more, or an absolute increase of 0.5 mg/dl or more in serum creatinine from baseline value, assessed at 48 hours following the administration of the contrast. The majority of the patients were overweight male ones with BMI 29.25.5 kg/m2. The primary endpoint of the study was the development of contrast-induced acute kidney injury according to KDIGO criteria. The prevalence of contrast-induced acute kidney injury was 12.9% (132 patients). 21.2% suffered from diabetes mellitus, 43% were obese and 12.9% had both diabetes mellitus and obesity. Diabetes wasnt a statistically significant independent risk factor of the contrast-induced acute kidney injury, as well as the combination of diabetes and obesity. In the group of obese patients the prevalence of contrast-induced acute kidney injury was higher (13.4%vs12.5%), but didnt meet statistical significance (p=0.7, OR 0.924, 95% CI 0.641.325). According to the multiple logistic regression model, female gender, age, BMI, weight, arterial hypertension, baseline creatinine were the risk factors of the contrast-induced acute kidney injury development (AUC 0.742,p0.0001). Diabetes mellitus was not associated with higher incidence of contrast-induced acute kidney injury. The prevalence of contrast-induced kidney injury was higher in the group of patients with BMI30 kg/m2, but didnt meet statistical significance and needs further evaluation in larger studies.

Diagnosis and prevention of contrast-induced acute kidney injury in coronary artery disease patients undergoing endovascular intervention

Introduction . In recent years, there has been a continuous increase in the number of endovascular interventions performed on the coronary arteries. Contrast-induced acute kidney injury is one of the main complications in patients who undergo coronary angiography and percutaneous coronary intervention (PCI). The filtration function of kidneys is usually evaluated by the level of endogenous creatinine or using calculation formulas also based on the concentration of creatinine. Plasma biomarkers, one of which is cystatin C, are the most promising for early detection of acute kidney injury. Purpose. (1) To evaluate the effectiveness of the prevention of contrast-induced kidney injury in patients administered with a loading dose of statins before endovascular intervention; (2) to study the prospects for early diagnosis of kidney injury using a new biomarker, cystatin C. Material and Methods . Patients with coronary artery disease, confirmed by еру hemodynamically significant stenosis of coronary arteries and clinically manifested angina pectoris, were selected. Before the endovascular intervention, patients were administered with loading doses of statins (group 1 received atorvastatin; group 2 received rosuvastatin). All patients underwent the following studies: general clinical examination; serial biochemical blood tests for creatinine, urea, uric acid, potassium, c-reactive protein, and cystatin C; and glomerular filtration rate assessment. Results. A decrease in renal function with a glomerular filtration rate of less than 60 mL/min/1.73 m 2 on day 5 was observed in 12 patients (34.3%) of group 1 and 9 patients (27.3%) of group 2. The blood study of cystatin C level allowed establishing an early diagnosis of contrast-induced acute kidney injury 12 and 24 h after endovascular intervention. Conclusions. A new biomarker, cystatin C, is a reliable indicator of kidney function. The anti-inflammatory effect, evaluated based on the high sensitivity c-reactive protein, was significantly more pronounced in coronary artery disease patients undergoing planned endovascular intervention and receiving loading doses of rosuvastatin compared to atorvastatin.

A Randomized Trial of Recombinant Human C1-Esterase-Inhibitor in the Prevention of Contrast-Induced Kidney Injury

ObjectivesThis study sought to determine the efficacy profile and safety of recombinant human C1 esterase inhibitor (rhC1INH) in the prevention of contrast-associated acute kidney injury after elective coronary angiography. BackgroundContrast-associated acute kidney injury is caused by tubular cytotoxicity and ischemia/reperfusion injury. rhC1INH is effective in reducing renal ischemia/reperfusion injury in experimental models. MethodsIn this placebo-controlled, double-blind, single-center trial 77 patients with chronic kidney disease were randomized to receive 50 IU/kg rhC1INH before and 4 h after elective coronary angiography or placebo. The primary outcome was the peak change of urinary neutrophil gelatinase-associated lipocalin within 48 h, a surrogate marker of kidney injury. ResultsMedian peak change of urinary neutrophil gelatinase-associated lipocalin was lower in the rhC1INH group (4.7 ng/ml vs. 22.5 ng/ml; p = 0.038) in the per-protocol population but not in the modified intention-to-treat analysis, and in patients with percutaneous coronary interventions (median, 1.8 ng/ml vs. 26.2 ng/ml; p = 0.039 corresponding to a median proportion peak change of 11% vs. 205%; p = 0.002). The incidence of a cystatin C increase ≥10% within 24 h was lower in the rhC1INH group (16% vs. 33%; p = 0.045), whereas the frequency of contrast-associated acute kidney injury was comparable. Adverse events during a 3-month follow-up were similarly distributed. ConclusionsAdministration of rhC1INH before coronary angiography may attenuate renal injury as reflected by urinary neutrophil gelatinase-associated lipocalin and cystatin C. The safety profile of rhC1INH was favorable in a patient population with multiple comorbidities. (Recombinant Human C1 Esterase Inhibitor in the Prevention of Contrast-induced Nephropathy in High-risk Subjects [PROTECT]; NCT02869347)