Contrast-Induced Acute Kidney Injury

McCullough, Peter A.

doi:10.1016/j.jacc.2007.12.035

Cited by 800 publications

(520 citation statements)

References 76 publications

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“…The primary outcome, CA-AKI, was defined as an increase of serum creatinine of 25% or 0.5 mg/dL or greater within 3 days after contrast administration [16]. Secondary outcomes included the KDIGO definition for AKI (a modification of the RIFLE and AKIN definition for AKI), defined as an increase of serum creatinine of 0.3 mg/dL or greater within a 48-h period or 50% or greater increase from baseline within 7 days [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…The most commonly used definition is an increase of serum creatinine C0.5 mg/dL or C25% from baseline, assessed 48-72 h after the procedure [16]. Recently, the Kidney Disease: Improving Global Outcomes (KDIGO) group defined a modified version of the definition for AKI that was previously developed by the Acute Dialysis Quality Initiative (ADQI) and the Acute Kidney Injury Network (AKIN) (http://www.KDIGO.org) [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Epidemiology of contrast-associated acute kidney injury in ICU patients: a retrospective cohort analysis

et al. 2011

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Intensive care unit (ICU) patients frequently undergo contrast-enhanced radiographic examinations, which carries a risk for development of contrast-associated acute kidney injury (CA-AKI). Data on this in ICU patients are scarce. The aim of this study was therefore to evaluate the epidemiology and short- and long-term outcomes of CA-AKI in ICU patients. A retrospective single-centre cohort study covering the period 1 March 2004 to 31 December 2008 on ICU patients who underwent a radiography examination with parenteral administration of iodinated radio contrast media was conducted. Data analysis included univariate and multivariate analyses of patients with and without CA-AKI. A total of 787 ICU patients were included in the study. CA-AKI occurred in 128 (16.3%) and was associated with higher need for RRT [30 (4.6%) vs. 21 (16.4%), p < 0.001], worse kidney function at discharge, longer length of ICU and hospital stay, and higher 28-day and 1-year mortality [28-day: 86 (13.1%) vs. 46 (35.9%), p < 0.001, and 1-year: 158 (24.0%) vs. 71 (55.5%), p < 0.001]. Higher serum creatinine, lower mean arterial pressure, and administration of diuretics and vasoactive therapy were associated with development of CA-AKI in multivariate analysis. After correction for confounders we found that CA-AKI was associated with 28-day mortality in this cohort of ICU patients (odds ratio = 2.742, 95% confidence interval 1.374-5.471). CA-AKI occurred in one out of six ICU patients who underwent a contrast-enhanced radiography examination and was associated with both short-and long-term worse outcomes such as need for RRT, worse kidney function at discharge, increased length of stay in the ICU and hospital, and mortality

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Epidemiology of contrast-associated acute kidney injury in ICU patients: a retrospective cohort analysis

et al. 2011

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“…SCr and CyC were measured at the time of admission and 24 to 48 hours after the procedure. CI‐AKI was defined by an absolute increase in SCr ≥0.3 mg/dL or relative increase in SCr ≥25% or CyC ≥10% over baseline 1, 14. Estimated glomerular filtration rate (eGFR) was calculated by applying the Modification of Diet in Renal Disease formula as modified by Levey 15.…”

Section: Methodsmentioning

confidence: 99%

“…Contrast‐induced acute kidney injury (CI‐AKI) is an important complication associated with cardiac catheterization 1. CI‐AKI accounts for a significant number of hospital‐acquired renal failure cases 2.…”

Section: Introductionmentioning

confidence: 99%

Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

Sun

Zhang

Ding

et al. 2016

JAHA

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BackgroundContrast‐induced acute kidney injury (CI‐AKI) is typically defined by an increase in serum creatinine after intravascular administration of contrast medium. Because creatinine is an unreliable indicator of acute changes in kidney function, we assessed whether circulating microRNAs (miRNAs) could serve as biomarkers for early detection of CI‐AKI.Methods and ResultsUsing a rat model of CI‐AKI, we first evaluated the miRNA profile of rat plasma and kidney. Three miRNA species with >1.5‐fold increase in plasma samples of CI‐AKI rats, including miRNA‐188, miRNA‐30a, and miRNA‐30e, were selected as candidate miRNAs. Quantitative real‐time polymerase chain reaction showed that these candidate miRNAs peaked in concentration around 4 hours after contrast medium exposure and were relatively renal‐specific. We compared the plasma levels of these candidate miRNAs in 71 patients who underwent coronary angiography or percutaneous coronary intervention and developed CI‐AKI with those of 71 matched controls. The plasma levels of the 3 candidate miRNAs were significantly elevated in the CI‐AKI group as compared to the control group. Receiver operating characteristic analysis showed that these miRNAs significantly distinguished patients with CI‐AKI from those without CI‐AKI. MiRNA composites were highly accurate for CI‐AKI prediction, as shown in maximized specificity by treble‐positive miRNA composite or maximized Youden index by any‐positive miRNA composite. Moreover, the selected miRNAs changes were associated with Mehran Risk Scores.ConclusionsPlasma levels of candidate miRNAs significantly distinguished patients with CI‐AKI from those without CI‐AKI. Thus, miRNAs are potential biomarkers for early detection of CI‐AKI.

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“…In these studies, AKI is frequently interpreted as CI‐AKI 1, 3. However, CI‐AKI is defined as an acute deterioration of renal function after administration of radiocontrast media in the absence of other alternative explanations for renal impairment 4, 5. Although this may be a reasonable assumption in patients undergoing elective PCI, deterioration of renal function after pPCI may be the result of multiple other contributing factors including hemodynamic alterations, neurohormonal activation, and initiation of nephrotoxic drugs.…”

Section: Introductionmentioning

confidence: 99%

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

Caspi

Habib

Cohen

et al. 2017

JAHA

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BackgroundAcute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast‐induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score–matched patients with ST‐segment–elevation myocardial infarction who were not exposed to contrast material.Methods and ResultsWe studied 2025 patients with ST‐segment–elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score–matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin‐treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra‐aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26).ConclusionsThe development of AKI in patients with ST‐segment–elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST‐segment–elevation myocardial infarction patients with and without contrast material exposure.

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Contrast-Induced Acute Kidney Injury

Cited by 800 publications

References 76 publications

Epidemiology of contrast-associated acute kidney injury in ICU patients: a retrospective cohort analysis

Epidemiology of contrast-associated acute kidney injury in ICU patients: a retrospective cohort analysis

Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

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