Does the Current Definition of Contrast‐induced Acute Kidney Injury Reflect a True Clinical Entity?

Abstract

Objectives: Contrast-induced acute kidney injury (CI-AKI) is defined as either a 25% increase in or an absolute elevation in serum creatinine (SCr) of 0.5 mg/dL, 48 to 72 hours after parenteral contrast exposure. The objective of this study was to compare the incidence and complications of AKI between patients exposed and those unexposed to intravenous (IV) contrast.Methods: This was a retrospective cohort study using the electronic medical record of adult patients (>18 years) with and without contrast-enhanced abdominal or chest computed tomography (CT) between May 2008 and April 2009. Inclusion criteria were emergency department (ED) patients with normal renal function who received either a contrast-enhanced abdominal or a contrast-enhanced chest CT, compared to those unexposed to IV contrast, with a repeat SCr within 48 to 72 hours. Exclusion criteria were contrast exposure within 7 days before the index visit. CI-AKI in the contrast-exposed group and AKI in the contrast-unexposed group were defined by the same changes in SCr 48 to 72 hours after contrast or ED admission. Data were described by proportions or medians with 95% confidence intervals (CIs) or interquartile ranges (IQR; 25% to 75%). Group comparisons were by Mann-Whitney U or Fisher's exact test (a = 0.05, two tails).Results: The contrast-exposed (n = 773) and contrast-unexposed (n = 2,956) patients were evenly matched for initial demographic, renal, and metabolic parameters. The incidence of CI-AKI/AKI was significantly higher for the patients unexposed versus exposed to contrast (8.96% vs. 5.69%, p = 0.003). There was no significant difference in mortality rates between contrast-exposed and unexposed patients (9.09% vs. 6.79%, p = 0.533). Conclusions:The definition of CI-AKI for ED patients with normal renal function may not represent a true clinical entity and the definition warrants revision.

Risk Factors for Radiocontrast Nephropathy After Emergency Department Contrast‐enhanced Computerized Tomography

“…The appropriateness of serum creatinine for the study of contrast nephropathy is actively debated, 29,30 with cystatin C, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 mentioned as potentially superior biochemical markers. 31 Even if such markers are better at assessing patients for RCN, however, testing for them is not routinely done in clinical practice, and they therefore could not be assessed in a large patient population such as the one we studied.…”

Does intravenous contrast-enhanced computed tomography cause acute kidney injury? Protocol of a systematic review of the evidence

“…Since 2008 (date on which the last study included in the more recent systematic review was published), several other studies measuring the effect of IV contrast medium on renal function were published [20,21,34,40-47]. Three among them [20,21,41] used propensity matching methods guaranteeing that the group exposed to IV contrast material and unexposed group had similar baseline characteristics and had a same likelihood of being exposed to IV contrast material.…”

Contrast‐induced Nephropathy: Doubts and Certainties

“…[13][14][15] In this article, Sinert et al compare their findings to those of a prospective ED-based study of patients by Mitchell et al, 16 undergoing contrast-enhanced computerized tomography, speculating that other inpatient causes of nephropathy likely contributed to the observed high rate of nephropathy in the study. 1,16 However, 51% of patients enrolled in the study by Mitchell were discharged from the ED, and the incidence of CIN (10%) was the same in both hospitalized and discharged patients. 16,17 The work by Sinert et al highlights the wide and deep gap in knowledge that separates current practice from an evidence-based approach.…”

“…I n this issue of Academic Emergency Medicine, Sinert et al 1 highlight three central controversies surrounding contrast-induced nephropathy (CIN): 1) does the current definition of CIN identify patients who have acute kidney injury (AKI) as a result of iodinated contrast-media exposure; 2) does a rise in creatinine following iodinated contrast exposure, that meets the definition of CIN, identify patients at increased risk of subsequent severe renal failure and death; and 3) does iodinated contrast cause clinically significant AKI 1 CIN results from the convergence of biochemical and pathophysiologic processes that initiate an insidious course with many parallels to other insidious diseases such as benign essential hypertension and diabetes mellitus. The initial stage is indolent and asymptomatic.…”