Volume-to-Creatinine Clearance Ratio

Laskey, Warren K.; Jenkins, Charles B.; Selzer, Faith; Marroquin, Oscar C.; Wilensky, Robert L.; Glaser, Ruchira; Cohen, Howard A.; Holmes, David R.; Investigators, Nhlbi Dynamic Registry

doi:10.1016/j.jacc.2007.03.058

Cited by 342 publications

(76 citation statements)

References 33 publications

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“…The reported incidence of AKI is 1% to 3% in patients undergoing elective PCI17, 19, 20, 21 but rises significantly to 10% to 16% in patients undergoing pPCI 3, 22, 23. The large increase in incident AKI is the result of heart failure, hemodynamic instability, and pharmacological interventions associated with STEMI rather than the use of greater contrast volume.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Even small volumes (∼30 ml) of contrast medium can have adverse effects on renal function in patients at particularly high risk [54]. As a general rule, the volume of contrast received should not exceed twice the baseline level of eGFR in ml [55]. This means for patients with significant CKD reasonable goals would be: <30 ml for diagnostic cardiac catheterization and <100 ml for PCI, CT, and other intravascular studies.…”

Section: Differences In Iodinated Contrastmentioning

confidence: 99%

Radiocontrast-Induced Acute Kidney Injury

McCullough¹

2008

Nephron Physiol

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Many radiographic studies and procedures use iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI). This is an important complication, which accounts for a significant number of cases of hospital-acquired renal failure associated increased hospital length of stay and increased mortality. Sustained reductions in renal blood flow, hypoxic injury, direct cellular toxicity by the contrast media, and superimposed organ injury are all believed to play a role in this form of AKI. Avoidance of dehydration and multimodality prevention measures may reduce rates of this problem in patients at risk. Contrast-induced AKI is likely to remain a significant challenge for specialists in the future since the patient population is aging, chronic kidney disease and diabetes are coming more common, and use of iodinated contrast is growing.

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“…Recent studies investigating the predictive value of the CV/eClCr or CV/eGFR ratios for CI-AKI suggested that maximally acceptable CV should be individually calculated by multiplying the cutoff value of the ratio and each patient's eGFR [1,4,5,6]. The use of eGFR with BSA normalization can lead to an underestimation of the actual contrast removal rate in overweighed individuals and to an overestimation in underweighted ones [12], so the use of raw eGFR without BSA normalization rather than BSA-normalized eGFR is more appropriate when dealing with the toxicity of contrast medium.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have demonstrated that the ratio of contrast volume (CV) to either estimated glomerular filtration rate (eGFR) or creatinine clearance (eClCr) can be used as a single risk predictor for contrast-induced acute kidney injury (CI-AKI), since this ratio pharmacokinetically means the area under the curve (AUC) representing the systemic exposure of a contrast agent to the body [1,2]. When dealing with pharmacokinetic issues, it is more appropriate to use the raw eGFR in absolute numbers (ml/min) individualized with the removal of body surface area (BSA) normalization.…”

Section: Introductionmentioning

confidence: 99%

Contrast Volume/Raw eGFR Ratio for Predicting Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention for Myocardial Infarction

Park

Kim

et al. 2015

Cardiorenal Med

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Background: Considering that contrast medium is excreted through the whole kidney in a similar manner to drug excretion, the use of raw estimated glomerular filtration rate (eGFR) rather than body surface area (BSA)-normalized eGFR is thought to be more appropriate for evaluating the risk of contrast-induced acute kidney injury (CI-AKI). Methods: This study included 2,189 myocardial infarction patients treated with percutaneous coronary intervention. Logistic regression analysis was performed to identify the independent risk factors. We used receiver-operating characteristic (ROC) curves to compare the ratios of contrast volume (CV) to eGFR with and without BSA normalization in predicting CI-AKI. Results: The area under the curve (AUC) of the ROC curve for the model including all the significant variables such as diabetes mellitus, left ventricular ejection fraction, preprocedural glucose, and the CV/raw modification of diet in renal disease (MDRD) eGFR ratio was 0.768 [95% confidence interval (CI), 0.720-0.816; p < 0.001]. When the CV/raw MDRD eGFR ratio was used as a single risk value, the AUC of the ROC curve was 0.650 (95% CI, 0.590-0.711; p < 0.001). When the CV/MDRD eGFR ratio with BSA normalization ratio was used, the AUC of the ROC curve further decreased to 0.635 (95% CI, 0.574-0.696; p < 0.001). The difference between the two AUCs was significant (p = 0.002). Conclusions: Raw eGFR is a better predictor for CI-AKI than BSA-normalized eGFR.

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Volume-to-Creatinine Clearance Ratio

Abstract: A V/CrCl ratio >3.7 was a significant and independent predictor of an early abnormal increase in serum creatinine after PCI in this unselected patient population.

Cited by 342 publications

References 33 publications

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

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

Radiocontrast-Induced Acute Kidney Injury

Contrast Volume/Raw eGFR Ratio for Predicting Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention for Myocardial Infarction

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