Acute kidney injury (AKI) is common among critically ill patients [
1]. Even mild forms are associated with significant mortality and morbidity [
2,
3]. Among the numerous causes of AKI in the intensive care unit (ICU), the toxicity of iodinated contrast media (CM) has been considered, for long, to be an important contributor, so called contrast-associated AKI (CA-AKI) [
2]. Indeed, the nephrotoxicity of iodinated CM is undisputed in experimental studies [
4]. However, in the clinical setting, several recent works suggest that, using modern low osmolarity iodinated CM, the incidence of AKI following exposition to CM is not higher than in matched non-exposed patients [
5‐
9]. In other words, there is increasing evidence of a minimal nephrotoxicity directly attributable to iodinated CM in the clinical setting of multifactorial renal aggression in the ICU, but also among general ward patients and in the emergency department [
5‐
12]. Early AKI detection is challenging as diagnosis is delayed until serum creatinine concentration rises and/or urine output decreases. Such delayed AKI diagnosis makes it difficult to assess the causal implication of CM among other renal aggressions. Performing a randomized trial testing CM versus placebo, albeit desirable to evaluate CM implication without any bias, would be ethically, at best, very difficult to perform. Thus, other methodologies, such as kidney aggression biomarkers analysis may be of value to complete the evidence provided by epidemiologic studies. Recently, in ICU patients, cell-cycle arrest biomarkers were identified as very promising for early detection of kidney aggression: the combination of tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor binding protein-7 (IGFBP-7) showed high sensitivity and specificity, outperforming other biomarkers for early detection of AKI [
13,
14]. To the best of our knowledge, the performance of [TIMP-2]·[IGFBP-7] has not been specifically evaluated in toxic AKI, despite some common pathophysiologic pathways shared among all AKI etiologies. Thus, quantifying cell-cycle arrest biomarkers before and after iodinated CM infusion as a direct evaluation of kidney aggression could be a means to confirm the recent, creatinine-based, epidemiologic evidence questioning the clinical relevance of CA-AKI. Furthermore, in the clinical setting of multifactorial kidney aggression, evaluating the effect of iodinated CM on those biomarkers is also important.
The aim of this preliminary study was to measure changes in TIMP-2 and IGFBP-7 urinary concentrations after iodinated CM-enhanced computed tomography in ICU patients.