Rates Of Contrast-induced Acute Kidney Injury Research Articles

A New Risk Factor Profile for Contrast-Induced Acute Kidney Injury in Patients Who Underwent an Emergency Percutaneous Coronary Intervention

We developed a new risk factor profile for contrast-induced acute kidney injury (CI-AKI) under a new definition in patients who underwent an emergency percutaneous coronary intervention (PCI). Consecutive patients (n = 1061) who underwent an emergency PCI were divided into a derivation group (n = 761) and a validation group (n = 300). The rates of CI-AKI were 23.5% (definition 1: serum creatinine [SCr] increase ≥25% in 72 hours), 4.3% (definition 2: SCr increase ≥44.2 μmol/L in 72 hours), and 7.0% (definition 3: SCr increase ≥44.2 μmol/L in 7 days). Due to the high sensitivity of definition 1 and the high rate of missed cases for late diagnosis of CI-AKI under definition 2, definition 3 was used in the study. The risk factor profile included body surface area <1.6 m2 ( P = .030), transient ischemic attack/stroke history ( P = .001), white blood cell count >15.00 × 109/L ( P = .047), estimated glomerular filtration rate <60 mL/min/1.73 m2 ( P = .002) or baseline SCr >133 μmol/L ( P = .007), intra-aortic balloon pump application ( P = .006), and diuretics administration ( P < .001), showing a significant predictive power in the derivation group and validation group. The new risk factor profile of CI-AKI under a new CI-AKI definition in emergency PCI patients is easily applicable with a useful predictive value.

Effect of the ischemic post-conditioning on the prevention of the cardio-renal damage in patients with acute ST-segment elevation myocardial infarction after primary percutaneous coronary intervention

Objective: To evaluate the effect of the ischemic post-conditioning (IPC) on the prevention of the cardio-renal damage in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PPCI). Methods: A total of 251 consecutive STEMI patients underwent PPCI in the heart center of Tianjin Third Central Hospital from January 2012 to June 2014 were enrolled in this prospective, randomized, control, single-blinded, clinical registry study. Patients were randomly divided into IPC group (123 cases) and control group (128 cases) with random number table. Patients in IPC group underwent three times of inflation/deflation with low inflation pressure using a balloon catheter within one minute after culprit vessel blood recovery, and then treated by PPCI. Patients in control group received PPCI procedure directly. The basic clinical characteristics, incidence of reperfusion arrhythmia during the procedure, the rate of electrocardiogram ST-segment decline, peak value of myocardial necrosis markers, incidence of contrast induced acute kidney injury(CI-AKI), and one-year major adverse cardiovascular events(MACE) which including myocardial infarction again, malignant arrhythmia, rehospitalization for heart failure, repeat revascularization, stroke, and death after the procedure were analyzed between the two groups. Results: The age of IPC group and control group were comparable((61.2±12.6) vs. (64.2±12.1) years old, P=0.768). The incidence of reperfusion arrhythmia during the procedure was significantly lower in the IPC group than in the control group(42.28% (52/123) vs. 57.03% (73/128), P=0.023). The rate of electrocardiogram ST-segment decline immediately after the procedure was significantly higher in the IPC group than in the control group (77.24% (95/123) vs. 64.84% (83/128), P=0.037). The peak value of myocardial necrosis markers after the procedure were significantly lower in the IPC group than in the control group(creatine kinase: 1 257 (682, 2 202) U/L vs. 1 737(794, 2 816)U/L, P=0.029; creatine kinase-MB: 123(75, 218)U/L vs.165(95, 288)U/L, P=0.010). The rate of CI-AKI after the procedure was significantly lower in the IPC group than in the control group(5.69%(7/123) vs. 14.06%(18/128), P=0.034). The rate of the one-year MACE was significantly lower in the IPC group than in the control group(7.32%(9/123) vs. 15.63% (20/128), P=0.040). Conclusion: The IPC strategy performed eight before PPCI can reduce myocardial ischemia- reperfusion injury, decline the rates of CI-AKI and one-year MACE significantly in STEMI patients, thus has a significant protective effect on heart and kidney in STEMI patients. Clinical Trial Registration Chinese Clinical Trials Registry, ChiCTR-ICR-15006590.

Risk of contrast-induced acute kidney injury in ST-elevation myocardial infarction patients undergoing multi-vessel intervention-meta-analysis of randomized trials and risk prediction modeling study using observational data.

Ascertaining risk of contrast induced acute kidney injury (CI-AKI) in ST-segment elevation myocardial infarction (STEMI) patients undergoing multi-vessel percutaneous coronary intervention (MV-PCI). Complete revascularization may improve outcomes in STEMI patients with multi-vessel disease. However, a practice of MV-PCI may be associated with a higher risk of CI-AKI. We aimed to evaluate the risk of CI-AKI in patients with STEMI and MV-PCI and examine the accuracy of a validated risk score. We searched PubMed, Cochrane Library, EMBASE, EBSCO, Web of Science, and CINAHL databases from inception through August 31, 2016 for randomized studies comparing CI-AKI rates with MV-PCI and infarct-related artery (IRA) only PCI during index hospitalization. A random effects model was used to estimate the risk ratio (RR) and respective 95% confidence intervals (CI). We queried the Nationwide Inpatient Sample (NIS) to assess the ability of the Mehran risk score to accurately predict the incidence of CI-AKI in patients undergoing MV-PCI. Four randomized studies (N = 1,602) were included in the final analysis. The risk of CI-AKI was low and no difference was observed with MV-PCI (1.45%) compared with IRA-only (1.94%) (RR 0.73, 95% CI 0.34-1.57; P = 0.57). From 2009 to 2012, excluding shock, there were 11,454 MV-PCI for STEMI patients in the NIS. The Mehran risk score accurately discriminated 78% of the patients who developed CI-AKI in this cohort (c-statistic of 0.78, P = 0.002). MV-PCI in STEMI is not associated with a higher risk of CI-AKI and the Mehran risk score can identify patients at higher risk for this complication. © 2017 Wiley Periodicals, Inc.

Metformin and contrast-induced acute kidney injury in diabetic patients treated with primary percutaneous coronary intervention for ST segment elevation myocardial infarction: Amulticenter study

AimTo analyze the association between chronic metformin treatment and the development of contrast-induced acute kidney injury (CI-AKI) after primary percutaneous coronary intervention (PCI) for ST segment elevation myocardial infarction (STEMI). MethodsPatients with type 2 diabetes mellitus (T2DM) treated with PCI <24h in 2 coronary care units were included. Serum creatinine (Cr) was measured before and <48h after PCI. CI-AKI was defined as an increase in Cr>27μmol/l (0.3mg/dl) or >50% over baseline after PCI. Since PCI was urgent, metformin could not be withheld prior to PCI but was usually stopped after PCI. ResultsAmong the 372 patients included, 147 (40%) were using metformin, which had older diabetes, but had risk factors similar to patients without metformin. Baseline eGFR was better in patients under metformin therapy. After PCI, we observed an increase of ≈10% in Cr, for both groups. There was a trend toward a lower rate of CI-AKI in patients under metformin (16% vs 25%, p=0.051). In patients with chronic kidney disease, 31 (26%) were under metformin therapy, and the rate of CI-AKI was similar in both groups (41% vs 40%, p=0.915). By multivariate analysis, metformin showed a trend toward a reduced rate of CI-AKI, even when adjusted for confounding (OR (95% CI): 0.548 (0.276–1.087)). No case of lactic acidosis was reported during the hospital stay. Moreover, there was no increased rate of cardiogenic shock or death with metformin treatment. ConclusionIn this multicenter observational study, chronic metformin treatment prior to primary PCI had no significant impact on CI-AKI.

Short-term rosuvastatin therapy prevents contrast-induced acute kidney injury in female patients with diabetes and chronic kidney disease: a subgroup analysis of the TRACK-D study.

Female patients are at higher risk of contrast-induced acute kidney injury (CIAKI) compared to males. In the multicenter, prospective, TRACK-D study, short-term rosuvastatin has proven effectively reduce CIAKI in patients with type 2 diabetes mellitus and stage 2-3 chronic kidney disease (CKD). This study aimed to explore the efficacy of rosuvastatin in the female TRACK-D population. This study was a gender-based analysis of 2,998 patients (1,044 females) enrolled in the TRACK-D study and were randomized to short-term (2 days before and 3 days after procedure) rosuvastatin therapy or standard of care. The primary outcome was the incidence of CIAKI and the secondary outcome was a composite of death, dialysis/hemofiltration or worsening heart failure at 30 days. CIAKI incidence was comparable between male and female patients in the overall study population (2.5% vs. 3.4%, P=0.165) and in the rosuvastatin group (2.4% vs. 2.1%, P=0.72), while it was higher in females than in males in the control group (3.1% vs. 5.3%, P=0.04). Female gender was an independent risk factor of CIAKI [odds ratio (OR) =1.65; 95% confidence interval (CI), 1.03-2.63; P=0.036]. Rosuvastatin treatment vs. control lowered CIAKI rate in females [2.1% vs. 5.3%; relative risk (RR) =0.39; 95% CI, 0.19-0.77; number needed to treat (NNT) =31], particularly among those with CKD stage 2 (1.2% vs. 4.1%, P=0.011). Secondary outcome incidence was similar for females in the rosuvastatin and control groups (3.7% vs. 4.9%, P=0.37). Compared to males, untreated females with diabetes mellitus and CKD had a higher risk of CIAKI, which can be reduced by short-term rosuvastatin treatment.

Economic impact of contrast-induced acute kidney injury associated with invasive cardiology: role of iso-osmolar contrast media in Germany, Italy, Poland, and Spain

Objective:Iso-osmolar Iodixanol is associated with a lower rate of contrast-induced acute kidney injury (CI-AKI) in patients at increased risk compared to low-osmolar contrast media (LOCM). The aim of this study was to assess the financial consequences of CI-AKI risk reduction in patients undergoing coronary angiography (CA) with or without percutaneous coronary intervention (PCI) in German, Italian, Polish and Spanish hospitals.Methods:This budget impact analysis (BIA) compared a scenario with iodixanol to a scenario without, where only LOCM were used, in patients at increased risk of CI-AKI over a 3-year horizon. A meta-analysis based on a systematic review observed a lower rate of CI-AKI with iodixanol compared to LOCM (Risk Reduction = 0.46) in patients with underlying impaired renal function (serum creatinine ≥1.6 mg/dl and estimated glomerular filtration rate ≤50 ml/min/1.73 m2). Contrast media and CI-AKI hospitalization costs were included in the analysis and unit costs were obtained from published literature, official sources or, when available, from hospital data. In the absence of country-specific data, resource utilization for a CI-AKI hospitalization was obtained by interviews with local clinicians in each country. The percentage of patients who received iodixanol was assumed to increase over time.Results:Based on a percentage of patients at increased risk of CI-AKI equal to 20% in Germany, 24% in Italy, 23% in Poland and 10% in Spain, results showed that the introduction of iodixanol would bring a 3-years cumulative net percentage saving on the total hospital budget of 29%, 34%, 25%, and 33% in the four countries respectively.Conclusion:The results of the analysis for the four countries showed that iodixanol use in patients at increased risk of CI-AKI undergoing CA with or without PCI may bring considerable savings on the hospital’s budget, due to the associated reduction in CI-AKI incidence.

Impact of Rosuvastatin in Contrast-Induced Acute Kidney Injury in the Elderly: Post Hoc Analysis of the PRATO-ACS Trial.

Age is a major predictor of contrast-induced acute kidney injury (CI-AKI). Few studies have focused on CI-AKI in elderly patients with acute coronary syndrome (ACS). We compare the incidence of CI-AKI in patients <75 and ≥75 years enrolled in the Protective effect of Rosuvastatin and Antiplatelet Therapy On contrast-induced acute kidney injury and myocardial damage in patients with ACS (PRATO-ACS) study and explore the impact of high-dose rosuvastatin on CI-AKI and clinical outcomes in the 2 age-groups. Statin-naive patients with non-ST-segment elevation ACS scheduled for early invasive strategy (total 504) were randomized to rosuvastatin (40 mg on admission followed by 20 mg/day) or no statin treatment. Contrast-induced acute kidney injury was defined as creatinine increase ≥0.5 mg/dL or ≥25% above baseline within 72 hours after contrast administration. All patients were stratified in tertiles according to baseline high-sensitivity C-reactive protein (hs-CRP). Rate of CI-AKI was significantly higher in patients ≥75 years (15.9% vs 8.7%, odds ratio: 2.001; 95% confidence interval: 1.14-3.53, P = .015). No significant interaction was observed between age and statin treatment (P = .17). Pretreatment with rosuvastatin was associated with 65% relative reduction in CI-AKI rate (22/170 [12.9%] vs 8/177 [4.5%], P = .007) in younger patients and 38% (16/82 [19.5%] vs 9/75 [12%], P = .20) in the elderly individuals. The greatest protective effect of statin treatment was achieved in patients with the highest hs-CRP values in both age-groups. Patients ≥75 years with ACS had a higher risk of developing CI-AKI. Early high-dose rosuvastatin is efficacious in reducing kidney injury in all patients, especially those with the highest baseline hs-CRP values.

Reducing contrast-induced acute kidney injury using a regional multicenter quality improvement intervention.

Contrast-induced acute kidney injury (CI-AKI) is associated with increased morbidity and mortality after percutaneous coronary interventions and is a patient safety objective of the National Quality Forum. However, no formal quality improvement program to prevent CI-AKI has been conducted. Therefore, we sought to determine whether a 6-year regional multicenter quality improvement intervention could reduce CI-AKI after percutaneous coronary interventions. We conducted a prospective multicenter quality improvement study to prevent CI-AKI (serum creatinine increase ≥0.3 mg/dL within 48 hours or ≥50% during hospitalization) among 21 067 nonemergent patients undergoing percutaneous coronary interventions at 10 hospitals between 2007 and 2012. Six intervention hospitals participated in the quality improvement intervention. Two hospitals with significantly lower baseline rates of CI-AKI, which served as benchmark sites and were used to develop the intervention, and 2 hospitals not receiving the intervention were used as controls. Using time series analysis and multilevel poisson regression clustering to the hospital level, we calculated adjusted risk ratios for CI-AKI comparing the intervention period to baseline. Adjusted rates of CI-AKI were significantly reduced in hospitals receiving the intervention by 21% (risk ratio, 0.79; 95% confidence interval: 0.67-0.93; P=0.005) for all patients and by 28% in patients with baseline estimated glomerular filtration rate <60 mL/min per 1.73 m(2) (risk ratio, 0.72; 95% confidence interval: 0.56-0.91; P=0.007). Benchmark hospitals had no significant changes in CI-AKI. Key qualitative system factors associated with improvement included multidisciplinary teams, limiting contrast volume, standardized fluid orders, intravenous fluid bolus, and patient education about oral hydration. Simple cost-effective quality improvement interventions can prevent ≤1 in 5 CI-AKI events in patients with undergoing nonemergent percutaneous coronary interventions.

Age, estimated glomerular filtration rate and ejection fraction score predicts contrast-induced acute kidney injury in patients with diabetes and chronic kidney disease: insight from the TRACK-D study

Background The occurrence of contrast induced acute kidney injury (CIAKI) has a pronounced impact on morbidity and mortality. The aim of the present study was to appraise the diagnostic efficacy of age, estimated glomerular filtration rate (eGFR) and ejection fraction (AGEF) score (age/EF(%)+1 (if eGFR was &lt;60 ml·min-1·1.73 m-2)) as an predictor of CIAKI in patients with diabetes mellitus (DM) and concomitant chronic kidney disease (CKD). Methods The AGEF score was calculated for 2 998 patients with type 2 DM and concomitant CKD who had undergone coronary/peripheral arterial angiography. CIAKI was defined as an increase in sCr concentration of 0.5 mg/dl (44.2 mmol/L) or 25% above baseline at 72 hours after exposure to the contrast medium. Post hoc analysis was performed by stratifying the rate of CIAKI according to AGEF score tertiles. The diagnostic efficacy of the AGEF score for predicting CIAKI was evaluated with receiver operating characteristic (ROC) analysis. Results The AGEF score ranged from 0.49 to 3.09. The AGEF score tertiles were defined as follows: AGEFlow ≤0.92 (n=1 006); 0.92 &lt;AGEFmid ≤1.16 (n=1 000), and ACEFhigh &gt;1.16 (n=992). The incidence of CIAKI was significantly different in patients with low, middle and high AGEF scores (AGEFlow=1.1%, AGEFmid=2.3% and AGEFhigh=5.8%, P &lt;0.001). By multivariate analysis, AGEF score was an independent predictor of CIAKI (odds ratio=4.96, 95% CI: 2.32–10.58, P &lt;0.01). ROC analysis showed that the area under the curve was 0.70 (95% CI: 0.648–0.753, P &lt;0.001). Conclusion The AGEF score is effective for stratifying risk of CIAKI in patients with DM and CKD undergoing coronary/peripheral arterial angiography. (Clinical Trial identifier: NCT00786136).

Continuous Venovenous Hemofiltration After Coronary Procedures for the Prevention of Contrast-Induced Acute Kidney Injury in Patients With Severe Chronic Renal Failure

Continuous venovenous hemofiltration (CVVH) is a renal replacement therapy that has been successfully used in patients with severe chronic renal failure to prevent contrast-induced acute kidney injury (CI-AKI). In this study, we present a consecutive experience using a new CVVH protocol that has also been applied to patients with acute coronary syndrome (ACS). CVVH was performed in consecutive patients with estimated glomerular filtration rate <30 ml/min/1.73 m(2) (mean ± SD, 21.1 ± 7.3 ml/min/1.73 m(2)) undergoing diagnostic or interventional coronary procedures starting after the angiographic procedures. Iopamidol was used as a contrast agent. In the first 6 patients, iopamidol removal by the CVVH hemofilter and kidney was calculated by measuring iopamidol concentrations in the blood, urine, and ultrafiltrate collected during the 6-hour CVVH session. In the second phase, the protocol was applied to 47 additional patients meeting the inclusion criteria. Six-hour CVVH resulted in iopamidol removal comparable with that of 12-hour diuresis (43 ± 12% vs 42 ± 15% of administered, p = NS). CI-AKI occurred in 7.5% of patients in the whole population and no patients had acute pulmonary edema, need for dialysis, or any major bleeding. In conclusion, in a population including patients with ACS with severe chronic renal failure undergoing coronary angiographic procedures, 6-hour CVVH performed only after contrast medium exposure was able to remove an amount of contrast medium similar to that removed by the kidneys in 12 hours and resulted in a low rate of CI-AKI.

A simple preprocedural score for risk of contrast‐induced acute kidney injury after percutaneous coronary intervention

To develop a simple scoring system based on preprocedural clinical features that is capable of predicting contrast-induced acute kidney injury (CI-AKI) before percutaneous coronary intervention (PCI). CI-AKI is associated with increased in-hospital morbidity and mortality, prolonged hospitalization, and long-term renal impairment. Although several scoring methods have been developed to determine risk of CI-AKI, no simple scoring method based on PCI preprocedural clinical features yet exists for Chinese patients. A total of 2,500 Chinese patients were randomly and retrospectively assigned in a 3:2 manner to create a training and validation dataset, respectively. CI-AKI was defined as an increase of ≥25% or ≥0.5 mg/dL serum creatinine within 5 days after PCI. Preprocedural clinical variables showing independent correlation to CI-AKI were used to derive the risk score from the training dataset and then subsequently tested in the validation dataset. The odds ratios from multivariate logistic regression were used to assign a weighted integer to age ≥70 years = 4, history of myocardial infarction = 5, diabetes mellitus = 4, hypotension = 6, left ventricular ejection fraction ≤45% = 4, anemia = 3, creatinine clearance rate <60 mL/min = 7, decreased high-density lipoprotein <1 mmol/L= 3, and urgent PCI = 3. Summation of the integers represented the total risk score. The overall incidence of CI-AKI in the training dataset was 16.4% [246/1500; 5.4% for low (≤7) and 61.3% for very high (≥17) risk scores]. The rates of CI-AKI, 1-year dialysis, and 1-year mortality increased significantly with each group (Cochran-Armitage test of trend, P < 0.001). The risk score facilitated appropriate classification of patients with low and high risk for CI-AKI after PCI in the validation dataset (c-statistic = 0.82). Risk classification based on the most significantly correlated parameters is useful for predicting CI-AKI before contrast exposure. The simple preprocedural score showed excellent predictive ability for identifying patients at high risk of nephropathy and those with deteriorative prognosis after PCI.

Impact of a High Loading Dose of Atorvastatin on Contrast-Induced Acute Kidney Injury

The role of statins in the prevention of contrast-induced acute kidney injury (CIAKI) is controversial. First, we investigated the in vivo effects of atorvastatin on CIAKI. Patients with chronic kidney disease enrolled in the Novel Approaches for Preventing or Limiting Events (NAPLES) II trial were randomly assigned to (1) the atorvastatin group (80 mg within 24 hours before contrast media [CM] exposure; n=202) or (2) the control group (n=208). All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution. Second, we investigated the in vitro effects of atorvastatin pretreatment on CM-mediated modifications of intracellular pathways leading to apoptosis or survival in renal tubular cells. CIAKI (ie, an increase >10% of serum cystatin C concentration within 24 hours after CM exposure) occurred in 9 of 202 patients in the atorvastatin group (4.5%) and in 37 of 208 patients in the control group (17.8%) (P=0.005; odds ratio=0.22; 95% confidence interval, 0.07-0.69). CIAKI rate was lower in the atorvastatin group in both diabetics and nondiabetics and in patients with moderate chronic kidney disease (estimated glomerular filtration rate, 31-60 mL/min per 1.73 m(2)). In the in vitro model, pretreatment with atorvastatin (1) prevented CM-induced renal cell apoptosis by reducing stress kinases activation and (2) restored the survival signals (mediated by Akt and ERK pathways). A single high loading dose of atorvastatin administered within 24 hours before CM exposure is effective in reducing the rate of CIAKI. This beneficial effect is observed only in patients at low to medium risk.

Impact of elevated serum glycated albumin levels on contrast-induced acute kidney injury in diabetic patients with moderate to severe renal insufficiency undergoing coronary angiography

BackgroundGlycated albumin (GA) has been shown to be a better indicator than glycosylated hemoglobin A1c (HbA1c) in terms of severity of renal impairment in patients with type 2 diabetes mellitus (T2DM). This study aimed to determine whether elevated serum GA levels are associated with an increased risk for contrast-induced acute kidney injury (CI-AKI) and worse clinical outcome in patients with T2DM and at least moderate renal insufficiency (RI) undergoing coronary angiography. MethodsSerum levels of fasting blood glucose (FBG), HbA1c and GA were measured in 1030 patients with T2DM and moderate to severe RI (eGFR 15–59mL/min/1.73m2). CI-AKI was defined as ≥25% increase in serum creatinine within 72h after the procedure. Receiver-operating characteristic curve was constructed to assess the predictive value of GA, HbA1c and FBG for CI-AKI. Multivariable logistic regression model was developed to identify risk factors for CI-AKI, and Kaplan–Meier curve analysis was used to compare the rates of dialysis and major adverse cardiac events (MACE) during one-year follow-up. ResultsThe overall rate of CI-AKI was 11.1%. GA was significantly higher in patients with CI-AKI than in those without, and correlated positively with changes of renal function after the procedure. After adjusting for age, sex, left ventricular ejection fraction, multi-vessel disease, type and volume of contrast media, FBG, and HbA1c, GA remained an independent risk factor for CI-AKI. GA≥21% was associated with increased rates of dialysis and MACE during one-year follow-up in patients with or without CI-AKI. ConclusionsIncreased GA level serves as a valuable risk factor for CI-AKI and indicates poor one-year clinical outcome in patients with T2DM and moderate to severe RI.

Sodium Bicarbonate Therapy for the Prevention of Contrast-Induced Acute Kidney Injury

Sodium bicarbonate has been postulated to prevent contrast-induced acute kidney injury (CI-AKI) by various mechanisms, although the reports are conflicting. We searched MEDLINE, EMBASE, and the Cochrane databases for randomized controlled trials that compared a sodium chloride with a sodium bicarbonate hydration regimen with regard to CI-AKI. Data across 19 clinical trials consisting of 3,609 patients were combined. Preprocedural hydration with sodium bicarbonate was associated with a significant decrease in the rate of CI-AKI (odds ratio [OR] 0.56; 95% confidence interval [CI] 0.36-0.86; P=0.008). Stratified analyses by the type of contrast medium suggested lower odds of CI-AKI with sodium bicarbonate in studies using low-osmolar contrast media (OR 0.40; 95% CI 0.23-0.71, P=0.002) compared with those using the iso-osmolar agents (OR 0.76; 95% CI 0.41-1.43; P=0.40). No significant difference in the rates of postprocedural death (OR 0.49; 95% CI 0.23-1.04; P=0.06) and the requirement for renal replacement therapy (OR 0.94; 95% CI 0.46-1.91; P=0.86) was observed. However, we found significant changes in serum bicarbonate and potassium levels after sodium bicarbonate infusion. This updated meta-analysis demonstrates that sodium bicarbonate-based hydration is superior to sodium chloride in preventing CI-AKI of patients undergoing exposure to iodinated contrast media.

Minimizing the Renal Toxicity of Iodinated Contrast

A substantial proportion of adults with coronary disease are at risk for contrast-induced acute kidney injury (CI-AKI), manifested primarily by underlying chronic kidney disease, defined as an estimated glomerular filtration rate <60 mL · min−1 · /1.73−2.1 Although patients commonly understand that they have heart disease, studies have shown that <10% of those with chronic kidney disease are actually aware of this problem; thus, if not emphasized by the cardiologist during the consent before angiography, CI-AKI may come as a surprise to patients and their families after the procedure.2–4 All forms of intravascular iodinated contrast are very water soluble, freely filtered by the glomerulus, and avidly taken up by renal tubular cells in the loop of Henle, and are retained in patients with chronic kidney disease within tubular cells and the peritubular space for ≈7 days where there is direct oxidative cellular damage, sloughing of renal tubular cells and brush border material, and acute tubular dysfunction.5 Thus, the interest in reducing CI-AKI and its translation, if …

How do centres begin the process to prevent contrast-induced acute kidney injury: a report from a new regional collaborative

ObjectivesThis study evaluates the variation in practice patterns associated with contrast-induced acute kidney injury (CI-AKI) and identifies clinical practices that have been associated with a reduction in CI-AKI.BackgroundCI-AKI is recognised...

C-Reactive Protein and the Risk of Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention

Background: The relationship between preprocedural C-reactive protein (CRP) levels and the incidence of contrast-induced acute kidney injury (CI-AKI) is unknown. Methods: Documents of 7,310 consecutive patients undergoing percutaneous coronary intervention (PCI) were screened. Patients with acute myocardial infarction, cardiogenic shock, concomitant inflammatory conditions or undergoing CABG within 48 h were excluded due to potential confounding effects. Results: A total of 4,522 patients were valid for analysis. The median follow-up was 26 months (interquartile range 20–33 months). According to preprocedural CRP values, patients were divided into 3 groups: group 1: CRP <1.0 mg/l (n = 1,523); group 2: 1.0 mg/l ≤ CRP ≤ 3.0 mg/l (n = 1,626); group 3: CRP >3.0 mg/l (n = 1,373). Patients with higher preprocedural CRP levels were associated with a significantly increased rate of CI-AKI (10.6 vs. 14.9 vs. 23.5%, p < 0.0001). After adjustment for baseline covariates, CRP level was still an independent predictor for the incidence of CI-AKI, either as a continuous variable or a categorical variable. Patients with higher CRP values had a significantly higher rate of all-cause mortality and myocardial infarction during follow-up. Conclusion: Elevated preprocedural CRP is associated with an increased risk for CI-AKI in patients undergoing PCI. Preprocedural risk stratification with CRP as an adjunct to established clinical risk factors might be useful.

Impact of contrast-induced acute kidney injury definition on clinical outcomes

Contrast-induced acute kidney injury (CIAKI) is a frequent complication after infusion of contrast media in patients undergoing percutaneous coronary intervention. A wide range of CIAKI rates occurs after intervention between 3% and 30%, depending on the definition. The aim of this study was to identify which methodology was more effective at recognizing patients at high risk for in-hospital and out-of-hospital adverse events. Serum creatinine increases, after contrast agent infusion, were evaluated in 755 consecutive and unselected patients. Incidences of CIAKI diagnosed by 2 common definitions varied from 6.9% (creatinine increase of ≥0.5 mg/dL, CIAKI-0.5) to 15.9% (creatinine increase of ≥25%, CIAKI-25%). Significant differences appeared between the 2 definitions of sensitivity to predict renal failure according to receiver operating characteristic curve analysis (98% for CIAKI-0.5 and 62% for CIAKI-25%), using a cutoff value of postprocedural glomerular filtration rate of 60 mL/min. Both definitions of CIAKI were related to composite adverse events, but CIAKI-0.5 showed a stronger predicting value (odds ratio 2.875 vs 1.802, P = .036). In multivariate linear regression, only CIAKI-0.5 was a predictive variable of death (odds ratio 3.174, 95% CI 1.368-7.361). An increase in serum creatinine of ≥0.5 mg/dL is more sensitive because it recognizes more selectively those patients with a higher risk of mortality and morbidity. Serum creatinine increases of ≥25% overestimate CIAKI by including many patients without postprocedural relevant deterioration of renal function and affected by a lower risk of adverse events at follow-up.

Renal insufficiency following contrast media administration trial II (REMEDIAL II): RenalGuard system in high-risk patients for contrast-induced acute kidney injury: rationale and design

The combined prophylactic strategy of sodium bicarbonate plus N-acetylsyteine (NAC) seems to be effective in preventing contrast induced acute kidney injury (CI-AKI) in patients at low-to-medium risk. However, in patients at high and very high risk the rate of CI-AKI is still high. In this subset of patients the anticipated advantages of the RenalGuard(tm) System should be investigated. The RenalGuard(tm) System (PLC Medical Systems, Inc., Franklin, MA, USA) is a real-time measurement and real time matched fluid replacement device designed to accommodate the RenalGuard therapy, which is based on the theory that creating and maintaining a high urine output is beneficial by allowing a quick elimination of contrast media, and, therefore, reducing its toxic effects. The REMEDIAL II trial is a randomised, multicentre, investigator-sponsored trial addressing the hypothesis that the RenalGuard System is superior to the prophylaxis with sodium bicarbonate infusion plus NAC in preventing CI-AKI in high and very high risk patients. Consecutive patients with chronic kidney disease (CKD) and at high to very high risk for CI-AKI, referred to our institutions for coronary and/or peripheral procedures, will be randomly assigned to 1) prophylactic administration of sodium bicarbonate plus NAC (control group) and 2) RenalGuard System treatment (RenalGuard group). All enrolled patients must have an estimated glomerular filtration rate ≤ 30 ml/min/1.73 m2 and/or a contrast nephropathy risk score ≥ 11. In all cases iodixanol (an iso-osmolar, non-ionic contrast agent) will be administered. The primary endpoint is an increase of ≥ 0.3 mg/dL in the serum creatinine concentration 48 hours after the procedure. The REMEDIAL II trial will give important answers on how to prevent CI-AKI in high and very high risk patients undergoing contrast media exposure.

Pre-Procedural Glucose Levels and the Risk for Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography

We sought to evaluate whether pre-procedural glucose levels are associated with contrast-induced acute kidney injury (CI-AKI) after coronary angiography. Although diabetes is a known risk factor for CI-AKI in patients undergoing coronary angiography, whether elevated pre-procedural glucose levels (regardless of pre-existing diabetes) are associated with higher risk for CI-AKI is unknown. We evaluated 6,358 patients with acute myocardial infarctions undergoing coronary angiography. Patients were stratified into 5 pre-procedural glucose groups: <110 mg/dl, 110 to <140 mg/dl, 140 to <170 mg/dl, 170 to <200 mg/dl, and >or=200 mg/dl. Logistic regression models were used to evaluate the relationship between glucose levels and risk for CI-AKI, first in the entire cohort and then in patients with and without established diabetes. The primary outcome was CI-AKI (>or=0.3 mg/dl absolute or >or=50% relative serum creatinine increase during 48 h after the procedure). The relationship between pre-procedural glucose and CI-AKI varied markedly in patients with and without diabetes. There was a strong association between glucose and CI-AKI risk in patients without diabetes (CI-AKI rates across the 5 glucose groups from lowest to highest: 8.2%, 9.9%, 12.4%, 14.9%, and 24.3%; p<0.001), but not in patients with diabetes (20.9%, 16.1%, 16.3%, 14.8%, and 19.2%, respectively; p=0.24; p for glucose x diabetes interaction<0.001). After adjusting for confounders (including baseline glomerular filtration rate), the relationship between higher glucose and greater CI-AKI risk persisted in patients without diabetes (odds ratios [95% confidence intervals] for glucose groups of 110 to <140 mg/dl, 140 to <170, mg/dl 170 to <200 mg/dl, and >or=200 mg/dl: 1.31 [1.00 to 1.71], 1.51 [1.11 to 2.10], 1.58 [1.03 to 2.43], and 2.14 [1.46 to 3.14] vs. glucose<110 mg/dl, respectively), but this relationship was not seen in patients with established diabetes. Elevated pre-procedural glucose is associated with greater risk for CI-AKI in patients without known diabetes who undergo coronary angiography in the setting of acute myocardial infarction. Measures used to prevent CI-AKI should be considered in these patients.