Published in:
01-01-2018 | Editorial
Contrast-associated acute kidney injury is a myth: Yes
Published in: Intensive Care Medicine | Issue 1/2018
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Contrast medium (CM) administration is widely cited as a leading cause of hospital-acquired acute kidney injury (AKI) [1]. Concern over precipitation of AKI by CM is pervasive, and has influenced clinical decision-making related to diagnostic imaging and therapeutic interventions for more than half a century. So-called contrast-induced AKI (CI-AKI) is defined as an acute impairment in renal function occurring within 3 days of CM administration that is not attributable to any other etiology [1, 2]. Yet, nearly all studies establishing CI-AKI as a clinical entity were performed in the absence of control populations not exposed to CM. These studies assumed causality from association, and considered all cases of AKI in CM-exposed patients as CI-AKI, even when alternative explanations were obvious (Fig. 1) [3‐5]. A growing body of evidence, derived from studies that include adequate control populations and discussed in more detail below, now suggests that risk for AKI attributable to CM administration is modest at most. Yet, outsized fear of CI-AKI persists.
Fig. 1
Diagram showing the importance of negative controls in evaluating the causal relationship between contrast media (CM) exposure and acute kidney injury (AKI). Regardless of the decision to use CM, acute illness (acute myocardial infraction, sepsis, trauma, etc.) produces a set of alternative conditions that can independently initiate the process of AKI prior to, during, and after the administration of CM. Note that the potential bias introduced by other causes of AKI increases with increasing severity of the acute illness. The essential purpose of the negative control group is to reproduce a condition that does not include the hypothesized causal mechanism but is very likely to involve the same sources of bias that are often present in the original association. If contaminants (source of bias) were responsible for the effect of the CM, they should exert their effect even when CM is not present. A control group allows us to estimate the true effect of CM exposure given the background of multiple confounders. In controlled studies, the outcome (AKI) is encountered without exposure to CM, demonstrating the existence of a confounding bias. AMI acute myocardial infarction, PE pulmonary embolism, PCI percutaneous coronary intervention, CT computed tomography, AKI acute kidney injury, CM contrast media, CKD chronic kidney disease
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