Iodinated Contrast Medium Renal Toxicity: The Phantom Menace or Much Ado About Nothing?

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We read with interest the article published in a recent issue of Critical Care Medicine by Valette et al (1). The authors report the lack of benefit of using sodium bicarbonate rather than isotonic sodium chloride for the prevention of iodinated contrast-associated acute kidney injury (CA-AKI).
In critically ill patients, as acknowledged by the authors, the cause of acute kidney injury (AKI) is multifactorial (sepsis, renal hypoxia, nephrotoxic medications, etc.). Therefore, the specific contribution of iodinated contrast medium (CM) to the kidney insult could hardly be delineated. The potential impact of preventive measures such as sodium bicarbonate is therefore uncertain. It is noteworthy that since first inclusions in the study by Valette et al (1) in 2012, a new trend has emerged concerning CA-AKI clinical relevance. Indeed, according to several very recent epidemiologic works among patients with (2, 3) or without critical illness (4), the prevalence of AKI following an imaging procedure appears similar in exposed and unexposed patients to iodinated CM. In other words, the contribution of iodinated CM to AKI in critically ill patients may have been overrated for years. However, in the absence of prospective randomized data, uncertainty remains. We believe the randomized trial by Valette et al (1) indirectly adds evidence reinforcing the findings of these epidemiologic studies. Indeed, alkalization with bicarbonate infusion is deemed to reduce CA-AKI by limiting CM-induced generation of free radicals, scavenging the potent oxidant peroxynitrate, and limiting the activation of inflammatory mediators (5). Hence, the lack of effect of targeting these pathways with bicarbonate infusion may suggest that they are only minimally activated by CM infusion. Studies failing at demonstrating the benefit of other preventive measures of CA-AKI, N-acetylcysteine for instance, could be interpreted the same way (5): targeting iodinated CM pathways of renal toxicity is useless since iodinated CM is not or only mildly culprit of the renal dysfunction. However, erroneous hypotheses about the mechanisms of iodinated CM renal toxicity or even unexplored pathways of this toxicity may also explain the lack of benefit of these specific preventive measures.
As there is undisputed evidence for renal toxicity of iodinated CM in the experimental setting (5), one may still fear that some patient subgroups may suffer such toxicity. Patients with multiple renal insults with already ongoing kidney dysfunction may represent such a high-risk population. Indeed, current guidelines underscore that “pre-existing renal functional impairment is the most important risk factor above all other risk factors for developing CA-AKI” (5). In this line, we regret that Valette et al (1) did not include patients with ongoing deterioration of renal function. Indeed, it is precisely in these patients, for whom physicians still dread administering iodinated CM, that assessing preventive strategies appears important. The inclusion of these patients and their separate analysis (even possibly underpowered) would have enabled to get the maximum of information out of the large trial performed by Valette et al (1). They should be congratulated for having conducted.
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