Intravascular Administration Of Contrast Media Research Articles

Navigating nephrotoxic waters: A comprehensive overview of contrast-induced acute kidney injury prevention

Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of acute kidney injury deriving from the intravascular administration of contrast media in diagnostic and therapeutic procedures and leading to longer in-hospital stay and increased short and long-term mortality. Its pathophysiology, although not well-established, revolves around medullary hypoxia paired with the direct toxicity of the substance to the kidney. Critically ill patients, as well as those with pre-existing renal disease and cardiovascular comorbidities, are more susceptible to CI-AKI. Despite the continuous research in the field of CI-AKI prevention, clinical practice is based mostly on periprocedural hydration. In this review, all the investigated methods of prevention are presented, with an emphasis on the latest evidence regarding the potential of RenalGuard and contrast removal systems for CI-AKI prevention in high-risk individuals.

Zero-contrast Multivessel Percutaneous Coronary Intervention with Intravascular Ultrasound Guidance in a Patient with Acute-on-chronic Kidney Disease: Turn Hopeless into Hopeful

Contrast-induced nephropathy is one of the serious complications in patients with renal dysfunction who underwent administration of intravascular contrast media. To overcome this, an approach of drastic reductions in contrast volume and the use of intravascular ultrasound has been adopted in some clinical cases. This report emphasizes the potential benefits of zero-contrast multivessel percutaneous coronary intervention in a patient presenting with acute-on-chronic kidney disease.

Radiographic Contrast Media and the Kidney.

AKI is a potential complication of intravascular iodinated contrast exposure. Contrast-associated AKI, which typically manifests as small and transient decrements in kidney function that develop within several days of contrast administration, is associated with serious adverse outcomes, including progressive kidney dysfunction and death. However, a causal link between the small increases in serum creatinine that characteristically occur with contrast-associated AKI and serious adverse outcomes remains unproven. This is important given mounting evidence that clinically indicated, potentially lifesaving radiographic procedures are underutilized in patients with CKD. This has been hypothesized to be related to provider concern about precipitating contrast-associated AKI. Intravascular gadolinium-based contrast, an alternative to iodinated contrast that is administered with magnetic resonance imaging, has also been linked with potential serious adverse events, notably the development of nephrogenic systemic fibrosis in patients with severe impairment in kidney function. Patients hospitalized in the intensive care unit frequently have clinical indications for diagnostic and therapeutic procedures that involve the intravascular administration of contrast media. Accordingly, critical care providers and others treating critically ill patients should possess a sound understanding of the risk factors for and incidence of such outcomes, the ability to perform evidence-based risk-benefit assessments regarding intravascular contrast administration, and knowledge of empirical data on the prevention of these iatrogenic complications.

Renal resistance index independently predicts worsening of renal function after coronary angiography

The renal resistance index (RRI) has been demonstrated to be a useful parameter that can detect patients at a high risk of worsening of renal function (WRF). This study was designed to evaluate the role of the RRI in predicting WRF mediated by the intravascular administration of contrast media. We enrolled patients who were referred for coronary angiography. Renal arterial echo-color Doppler was performed to calculate the RRI. WRF was defined as an increase of > 0.3 mg/dL and at least 25% of the baseline value in creatinine concentration 24–48 h after coronary angiography. Among the 148 patients enrolled in this study, 18 (12%) had WRF. In the multivariate logistic analysis, the RRI was independently associated with WRF (odds ratio [OR]: 1.22; 95% confidence interval [CI]: 1.09–1.36; p = 0.001). After angiography, the RRI significantly increased in both patients with and without WRF. In the receiver operating characteristic curve analyses for WRF, the RRI at baseline and after angiography showed similar accuracy, and the best cutoff value for predicting WRF was 70%. In patients undergoing coronary angiography, the RRI is independently associated with WRF, probably because it provides more accurate information about cardiorenal pathophysiological factors and reflects kidney hemodynamic status and flow reserve.

P243 RELEVANCE OF RENAL RESISTANCE INDEX INCREASE AFTER CORONARY ANGIOGRAPHY

Abstract Background Renal resistance index is a Doppler derived measure which is able to reflect the pathophysiological background of Cardiorenal Syndrome (CS). There are no data about the influence of the intravascular administration of contrast media on RRI and its relationship with worsening of renal function (WRF). Aim of the Study To evaluate changes in renal resistance index (RRI) after coronary angiography in patients with and without WRF. METHODS We enrolled 115 patients (mean age 64 years, 73% males, 84% hypertensive, 43% diabetic, 30% with acute coronary syndrome, 21% affected by chronic heart failure, CHF, with a mean left ventricular ejection fraction, LVEF, of 51±11) with suspected coronary artery disease, stable angina, or acute coronary syndromes who have been referred for coronary angiography (with or without pre–existing renal impairment). Renal arterial echo–color Doppler was used to calculate RRI before and 48 hours after coronary angiography. WRF was defined as an increase of creatinine >0.3 mg/dl and of at least 25% from baseline 24–48 hours after coronary angiography. Results Fourteen (12%) among the enrolled patients showed WRF. As expected, a significant increase of creatinine serum levels was observed in patients with WRF (from 1.14±0.40 to 1.71±0.49, p < 0.001) but not those without (from 0.89±0.27 to 0.92±0.28, p n.s.) WRF. On the other hand, RRI significantly increased both in patients with (from 72.8±4.3 to 76.4±5.2, p < 0.05) and without (from 63.1±7.2 to 65.4±7.1, p < 0.05). However, both at baseline and after angiography, patients with WRF showed RRI values significantly greater when compared with those without. At ROC curve analyses for WRF, the baseline and after angiography RRI sowed similar AUC (0.88 and 0.90, respectively) and for both RRI values the best cut–off was 70% (sensitivity of 79% and 93% and Specificity of 93% and 82%, respectively). As shown in the figure, the high predictive accuracy of RRI values was due to the fact that, although increased after angiography, the proportion of patients without WRF and with RRI>70% remained very low. Conclusion After coronary angiography RRI significantly increase both in patients with and without WRF. However, a larger proportion of patients with WRF present a critically increased RRI, i.e. equal or above 70%, before and after angiography probably because reflecting the pathophysiological background underlying the progression of cardiorenal syndrome.

Vitamin C in the Prevention of Contrast-induced Nephropathy among High-risk Patients Undergoing Coronary Angiogram: A Meta-analysis

Background: Contrast-Induced nephropathy (CIN) is one of the leading causes of acute kidney injury. The most common procedures associated with CIN are coronary angiography and contrast enhanced computed tomography (CT) [1]. The most common definition in use is an increase in serum creatinine (SCr) of >25% of the baseline values occurring following the intravascular administration of contrast media without an alternative explanation [2]. Generation of reactive oxygen species is thought to play a role in the pathogenesis of CIN, hence researches have been conducted into the potential role of antioxidants in the prevention of contrast-induced nephropathy [3]. Vitamin C, a potent antioxidant in humans has the ability to oxidize free radicals, and has been studied in different trials to measure its ability to prevent CIN among patients undergoing coronary angiogram.
 Objective: To determine if vitamin C prevents CIN among High-risk patients (Creatinine Clearance <60 ml/min/m2, Diabetics, and on administration of high-volume contrast media).
 Methodology: All studies, limited to randomized clinical trials were sought for this analysis through PubMed, the Cochrane Library, ClinicalTrials.gov. Database was searched using the terms “vitamin C”, “Prevention”, “acute kidney injury” and “contrast-induced nephropathy”. Adult patients (40-90 years old) with Creatinine Clearance of <60 ml/min/m2 or baseline creatinine >1.2 mg/dl, Diabetes Mellitus Type II, and were administered with high-volume contrast media (>100ml) undergoing coronary angiogram were included in the study. Exclusion Criteria were patients with normal baseline renal function, without risk factors for CIN, with EGFR < 30 ml/min/m2, with regular intake of Vitamin C and were on dialysis. Statistical data were obtained using Review Manager (RevMan) Version 5.3 freeware program. P Value was obtained using the Cochran–Mantel–Haenszel test (CMH). Included patients were given Vitamin C at doses of 1 gram to 3 grams, taken orally or administered intravenously pre-and post coronary angiogram.
 Results: Seven hundred and one (N=701) patients were included in this meta-analysis. CIN occurred in 3.5% of patients (N=25) in the ascorbic acid group and in 6% of patients (N= 42) in the placebo group (p value of 0.03).
 Conclusion: Vitamin C given at doses 1 gram to 3 grams in combination with hydration prior to coronary angiogram may have a significant effect in the prevention of CIN in high-risk patients.

Prevention of contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention.

Intravascular administration of contrast media is an irreplaceable step of percutaneous coronary intervention. Since the latter is a very common procedure, contrast‑induced acute kidney injury (CI‑AKI) has become one of the most frequent causes of acute nephropathy, and a relevant prognostic impact of CI‑AKI has been observed. Some patient comorbidities and procedural characteristics have been identified as key risk factors of CI‑AKI. In this review, we discuss current evidence and future research directions on CI‑AKI prevention in patients undergoing percutaneous coronary intervention.

Contrast-induced nephropathy: A dilemma between loss of neurons or nephrons in the setting of endovascular treatment of acute ischemic stroke.

The aim is to report the incidence and risk factors of contrast-induced nephropathy after the use of iodine-based contrast for the endovascular treatment of acute ischemic stroke. Data from patients who underwent neuroendovascular procedures in a center over a period of 22 months were analysed retrospectively. Contrast-induced nephropathy was determined by an increase in serum creatinine level of >25% of baseline or an absolute increase in serum creatinine level of at least 44 µmol/L (0.50 mg/dL) occurring after intravascular administration of contrast media without alternative explanation. The primary outcome measure of this study was the presence of contrast-induced nephropathy in these treated patients. Continuous data were presented as mean ± standard deviation, and categorical data as frequencies or percentages. The comparison was made using Student's t-test or Fisher's test. Logistic regression was performed to find independent contrast-induced nephropathy predictors. All statistical analyses were performed using Microsoft Excel. A p value of less than 0.05 was considered statistically significant. One hundred and eighty-nine patients undergoing endovascular treatment for acute ischemic stroke. Twenty cases of the total cohort (n = 189) presented contrast-induced nephropathy (10.58%). Only diabetes and creatinine levels between 1.3 and 2.5 mg/dL were associated with contrast-induced nephropathy. No patient was treated with dialysis. Contrast-induced nephropathy is a relatively common complication after endovascular treatment of acute ischemic stroke and is associated with worse outcome in patients with this condition. However, there is no increase in the frequency of hemodialysis after the use of iodinated contrast medium.

EVALUATION OF BLOOD PRESSURE VARIATIONS DURING THE ADMINISTRATION OF INTRAVASCULAR CONTRAST MEDIA IN CECT ABDOMEN

Objective: Hemodynamic changes may occur with the rapid intravenous injection of contrast media due to the osmolality of contrast media. This study is aimed to evaluate the blood pressure variation during the administration of intravascular contrast media in contrast-enhanced computed tomography (CECT) of the abdomen.Methods: The study was performed in 146 subjects, who underwent abdomen CT scan with 64-slice Philips Brilliance CT scanner in the department of radio-diagnosis and imaging. Using convenience sampling technique, 73 subjects who were referred for CECT abdomen scan and another 73 subjects who were referred for non-CECT (NCECT) abdomen scan were included in the study. Among the CECT group, intravascular contrast media was injected into the patient during the scan. Both systolic and diastolic blood pressures were recorded just before and immediately after the scan in CECT and NCECT groups, by two readers independently. Mean systolic and diastolic blood pressure for both groups was calculated with standard deviation. The data were analyzed using repeated measures of ANOVA.Results: Both systolic and diastolic blood pressures increased with the injection of contrast media among CECT scan group. No significant changes in systolic and diastolic blood pressure were found before and after the scan of NCECT group.Conclusion: An increase in both systolic and diastolic blood pressures is associated with the intravascular administration of non-ionic low-osmolar contrast media.

The role of thiol levels in predicting contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention.

OBJECTIVE:Contrast-induced nephropathy (CIN) is a common complication of diagnostic or interventional procedures that may arise from administration of intravascular contrast media. Recent studies have reported the thiol-disulfide ratio as a novel oxidative stress marker. Therefore, we investigated the role of thiol levels in predicting CIN in patients with ST-segment elevation myocardial infarction (STEMI) who had undergone primary percutaneous coronary intervention (PCI).METHODS:A total of 302 patients were enrolled in the study. CIN was defined as an increase in serum creatinine concentration ≥0.5 mg/dL compared with the admission value or a >25% relative rise during the first 48–72 hours after the procedure. To evaluate the relationship between thiol levels and CIN, the patients were divided into a CIN group and a non-CIN group.RESULTS:CIN occurred in 44 (15%) patients. Native thiol (274.8±84.7 μmol/L vs. 220.8±97.1 μmol/L, p=0.001) and total thiol (305.4±89.7 μmol/L vs. 260.1±102.1 μmol/L, p=0.009) levels were higher in patients within the non-CIN group. Disulfide (15.8±6.6 μmol/L vs. 19.6±8.4 μmol/L, p=0.002) levels, and mean disulfide/total thiol ratios (8.4±3.7 vs. 5.9±3.1, p=0.001) were higher in patients with CIN (+) group. In univariate analysis, the initial native thiol, total thiol, disulfide levels, and disulfide/total thiol ratio were found to have prognostic significance in the development of CIN. In the multivariate regression analysis, only the disulfide/total thiol ratio (OR=1.190; 95% CI: 1.090–1.300; p=0.001) was significantly and independently associated with CIN. The cutoff value of the disulfide/total thiol ratio to predict CIN on admission in patients with STEMI who underwent primary PCI was 7, with a sensitivity of 68.2% and a specificity of 79.8%.CONCLUSION:Our results suggest that thiol/disulfide homeostasis could be a good biochemical risk marker for CIN in STEMI patients who underwent primary PCI.

Contrast-induced acute kidney injury in cardiology

The intravascular administration of contrast media is an important tool in cardiovascular imaging, especially in percutaneous coronary interventions (PCI). Owing to the widespread use of these procedures, contrast-induced acute kidney injury (CI-AKI) has become one of the most common types of acute renal failures. CI-AKI is mainly mediated by mechanisms of oxidative damage, and its onset is associated with prolonged hospitalization and significant morbidity and mortality. Preexisting chronic kidney disease, diabetes, age, heart failure, and characteristics related to the procedure (primary or elective PCI, type and amount of contrast medium) are the most important risk factors for the development of post-PCI CI-AKI.For this serious complication, prevention is more important than treatment, and various preventive measures have been widely tested in recent years. However, none of the strategies so far evaluated, with the exception of pre-procedural hydration with isotonic saline, has been shown to effectively prevent CI-AKI in randomized trials in large populations. In this review, we discuss the incidence, risk factors, main pathogenetic mechanisms and current strategies for the prevention of CI-AKI.

Prevention of Contrast-Induced Acute Kidney Injury: an Update.

Contrast-induced acute kidney injury (CI-AKI) is a common complication of intravascular administration of contrast media used in coronary angiography, percutaneous coronary intervention and other diagnostic and interventional procedures. This review article aims at summarizing the published literature regarding the prevention of CI-AKI, by focusing on available high-quality meta-analyses addressing this matter. Apart from adequate hydration, a number of pharmacologic agents have been proposed as potential candidates to be included in the routine preparation, prior to the patient's arrival in the cardiac catheterization laboratory. Among them, statins and N-acetylcysteine appear to be the most extensively studied ones. Throughout this article we present the available data on CI-AKI prevention and provide a critical clinical appraisal, as well as a summary of currently available guidelines.

Contrast-induced nephropathy (reference review and the author’s own findings)

This review shows the frequency of incidence of contrast-induced nephropathy in patients with ischemic heart disease who underwent percutaneous coronary intervention with intravascular administration of contrast media. The information about the pathogenesis, risk stratification and clinical manifestations of contrast-induced nephropathy is presented. Also, results of current completed studies about the possible therapeutic measures aimed at the prevention of this nephropathy are shown in this review.

Contrast medium-induced nephropathy, a more practical approach to prevention?

To The Editor: we read with interest the good review article by Drs Sterner and Nyman [1] concerning the safe use of intravascular contrast medium for both coronary interventions and multi- channel detector computed tomography. As a radiology department in the United Kingdom, our current policy is to follow specific guidelines issued by the Royal College of Radiologists [2] When compared, the two publications hold many similarities with respect to their recommendations for clinical practice. This is especially true with the recommendations for optimising the patient's renal state prior to any procedure requiring the administration of intravascular contrast media. However, on a practical note, we would suggest that the different calculations proposed to determine the Glomerular Filtration Rate [3–5] are too complex for use in every patient requiring intravascular contrast medium. As a department, we continue to use baseline creatinine levels as a screening tool in high risk patients (i.e. the elderly and patients with a history of diabetes and/or renal disease). We have found this to be sufficient. A review paper by P. Aspelin [6] conveys a very similar message but perhaps in a more general physician-orientated approach. His concluding recommendations are simple: confirm the need for contrast media, identify the at risk patient, hydrate adequately, discontinue nephrotoxic drugs before the procedure, and choose a contrast medium with the lowest nephrotoxic effects. These simple guidelines are perhaps more appropriate for day- to-day practice and for general distribution to referring clinicians who may be deterred by the more complicated equations in the other publications.

Contrast medium-induced nephropathy: The pathophysiology

A widespread, rather general, definition of contrast-induced nephropathy (CIN) is an impairment in renal function occurring within 3 days following the intravascular administration of contrast media (CM) and the absence of an alternative aetiology. In spite of the vast clinical importance of CIN, its understanding and the pathophysiology behind CIN remain incomplete. Many studies have been performed; however, they have provided no widely accepted conclusion so far. Here the possible mechanisms underlying CIN are outlined, which span from altered rheological properties, perturbation of renal haemodynamics, regional hypoxia, auto-, and paracrine factors (adenosine, endothelin, reactive oxygen species) to direct cytotoxic effects. Although these potential mediators of CIN will be discussed separately, several factors may act in concert to perturb kidney function after exposure to contrast media. From the current knowledge of the mechanisms causing CIN, it is not possible to recommend a certain class of contrast media, except to avoid large doses of CM of the first generation. From a pathophysiological perspective, volume expansion is effective in avoiding CIN, since water permeability of the collecting ducts will decrease and enhance fluid excretion. Hence, CM in the distal portions of the tubular system is diluted, which implies reduced fluid viscosity and a lower risk of obstruction.

ASGE Technology Status Evaluation Report: radiographic contrast media used in ERCP

ASGE Technology Status Evaluation Report: radiographic contrast media used in ERCP

Statin therapy reduces contrast-induced nephropathy: An analysis of contemporary percutaneous interventions

Purpose We sought to examine whether statin therapy before percutaneous coronary intervention results in reduction in contrast-induced nephropathy (CIN). Intravascular administration of contrast media can have nephrotoxic effects, particularly in patients with baseline renal insufficiency. Along with lowering serum cholesterol, statins have pleiotropic effects in the vasculature. The effect of statin use on CIN is unknown. Subjects and methods We studied 29 409 patients who had both baseline preprocedure and peak postprocedure serum creatinine measured at the time of their percutaneous coronary intervention (PCI). Baseline demographics and creatinine profile before and after the procedure were compared between patients who received preprocedure statins and those who did not. CIN was defined as an increase in serum creatinine of ≤0.5 mg/dL. Results Baseline serum creatinine was similar between the two groups. When compared with patients who did not receive preprocedure statins, patients on preprocedure statins had a lower incidence of CIN (4.37 vs 5.93, P <0.0001) and nephropathy requiring dialysis (0.32 vs 0.49, P = 0.03). After adjustments for comorbidities, preprocedure statin use was associated with a significant reduction in CIN (odds ration [OR] 0.87, 95% confidence interval [CI] 0.77–0.99, P = 0.03). Conclusions Preprocedure statin use is associated with significant reduction in CIN after contemporary PCI. This reinforces the need to initiate statin therapy before percutaneous coronary interventions.

Ureteric obstruction and intravascular administration of contrast media: is there a risk?

Experimental studies in animal models have shown that acute ureteric obstruction for 24 h or more is associated with a decrease in renal medullary blood flow and structural damage to the tubules [1, 2]. Does intravascular administration of contrast medium (CM) in the presence of acute ureteric obstruction induce further damage to the kidney? Clinical data on this subject are lacking and there is only one experimental study in the rat that has investigated this issue extensively [1]. The results of this study demonstrated that the combination of acute ureteric obstruction, inhibition of intrarenal production of the vasodilators nitric oxide (NO) and prostacycline, and intravascular administration of high osmolar CM results in extensive necrosis of the medullary thick ascending limb of loops of Henle (mTALs) [1]. The combination of insults used in the rat is not uncommon in patients suffering from acute renal colic secondary to ureteic obstruction caused by a calculus. These patients may undergo intravenous urography to determine the cause of the renal colic. Intravascular administration of CM can induce reduction of renal blood flow and a hypoxic insult to the renal medulla [3–7]. A patient with renal colic may also receive non steroidal anti-inflamatory drugs (NSAIDs) such as indomethacin for pain relief and smooth muscle relaxation. These drugs cause inhibition of intrarenal production of the vasodilator prostacycline, causing a marked decrease in medullary renal blood flow that may lead to necrosis of mTALs [1, 3]. In addition, some of these patients may be suffering from endothelial dysfunction associated with hypertension, atherosclerosis or diabetes mellitus. This causes a reduction in endogenous production of the vasodilators NO and prostacycline, which are crucial for perfusion of the renal medulla [3–7]. In this short communication, the pathophysiology of ureteric obstruction and the medullary effects of contrast media will be discussed. The harmful combination of ureteric obstruction, use of NSAIDs and intravascular injection of CM will be highlighted.

Contrast media-induced nephrotoxicity--questions and answers.

The intravascular administration of contrast media (CM) can produce acute haemodynamic changes in the kidney characterized by an increase in renal vascular resistance and a decrease in the glomerular filtration rate (GFR). These changes may lead to clinically significant reduction in renal function in patients with pre-existing risk factors such as diabetic nephropathy, congestive heart failure and dehydration. The pathophysiology of the renal haemodynamic effects of CM involves activation of the tubuloglomerular feedback (TGF) mechanism and the modulation of the intrarenal production of vasoactive mediators such as prostaglandins, nitric oxide, endothelin and adenosine. The TGF response is osmolality-dependent and accounts for about 50% of the acute functional effects of high osmolar CM on the kidney. Reduction in the synthesis of the endogenous vasodilators nitric oxide and prostaglandins increases the nephrotoxicity of CM. Endothelin and adenosine play a crucial role in mediating the acute functional effects of CM. Antagonists of these mediators attenuate the reduction in renal function induced by contrast agents. Vacuolization of the cells of the proximal tubules and necrosis of those of the medullary ascending limbs of loops of Henle are the main structural effects of CM in the kidney. The reduction in renal function induced by CM could be minimized by the use of low osmolar CM and adequate hydration. The prophylactic administration of calcium channel blockers and adenosine antagonists such as theophylline may also offer some protective effect.

Tubular toxicity is the main renal effect of contrast media.

The aim of this study is to evaluate the effects of contrast media on both tubular and glomerular function. Different parameters of tubular and glomerular function were determined before and at 1, 3, and 5 days after the intravascular administration of contrast media in 100 adult renal patients (plasma creatinine 0.6-10.8 mg/dL, mean: 1.3). Urinary activities of five tubular enzymes (alanine aminopeptidase, gamma-glutamyltransferase, alkaline phosphatase, lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase) increased significantly on the first day after the administration of contrast media, indicating a tubular damage. Glomerular filtration rate and the conventional tests of glomerular function (plasma creatinine, creatinine clearance, and urinary proteins) presented only slight variations after the administration of contrast media. In conclusion, contrast media principally affected the renal tubule (as demonstrated by enzymuria), while their effects on glomerular function were very mild.