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Iodinated contrast and acute kidney injury: major culprit or innocent bystander? Time for reappraisal.

Critical Care Medicine www.ccmjournal.org 1149 Contrast-induced nephropathy (CIN) is a major cause of hospital-acquired acute kidney injury (AKI). Its prevalence is highly variable, which is linked to the studied populations’ baseline characteristics and comorbidities and to the lack of uniformity in definitions used (1). The overall prevalence is estimated between 1% and 30% of patients receiving iodinated contrast medium (CM). Decreased baseline glomerular filtration rate, diabetes, heart failure, hypotension, dehydration, and older age, with the type and amount of CM, are the main recognized risk factors. Patients in the ICU have frequently multiple, often unavoidable, AKI risk factors (sepsis, shock, and nephrotoxic medications), undergo the growing use of imaging and interventional procedures (2), and are more and more older (3). Thus, they seem particularly exposed to CIN. Until very recently, data on CIN in ICU patients were rather scarce. In two retrospective studies, the prevalence has been evaluated at 16.3% in surgical ICU patients and at 14% in medical ones (4, 5). The prevalence was 19% in a prospective study among surgical patients (6). Because of the usual multifactorial origin of AKI in the ICU, no conclusion concerning the relationship between CM infusion and renal function impairment can be drawn from these studies. With the exception of one small sample study (where CIN prevalence was very low, and its definition very different from the usually accepted ones) (7), no results comparing the prevalence of AKI in the presence or absence of CM infusion in ICU patients have been published. That is precisely what Ehrmann et al (8) did in their study published in this issue of Critical Care Medicine. The authors assessed the prevalence and mortality of monomeric nonionic low-osmolar CM-associated AKI in two ICUs. They studied prospectively a cohort of 380 patients (with a large case mix including medical, trauma, and surgical ones) composed by 307 expositions to CM and 170 control expositions (imaging without CM or intrahospital transport). Their main result was that the use of monomeric nonionic low-osmolar CM agents did not affect the prevalence of AKI nor the hospital mortality. Indeed, some limits apply to this work. First, definitive conclusion can be drawn from the mortality analysis, and data concerning long-term outcomes are lacking. Second, control inclusions were largely represented by patients who underwent imaging procedures without CM infusion. Among them, it cannot be excluded that the decision not to use CM may be linked to a presumed high risk of CIN. Furthermore, increase in serum creatinine concentration has already been described in noncritically ill patients who had CT scan without CM administration (9). Finally, large proportion of patients treated with one or more nephrotoxic medications (excluding CM) may have contributed to dilute the specific role of CM in the occurrence AKI. The direct role of CM in AKI in critically ill patients remains unclear. Further prospective studies on CIN, using a consensual definition (as done for AKI of other causes) for the sake of clarity and uniformity, are needed. Until more results become available, the exact role of CM, ranging from major culprit to innocent bystander, will remain questionable.