Abstract
BackgroundIodinated contrast media may contribute to acute kidney injury. However, several recent works suggest that this toxicity is minimal in the clinical setting. Recently, urinary G1 cell-cycle arrest proteins tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin like growth factor binding protein 7 (IGFBP-7) were identified as highly sensitive and specific biomarkers for early detection of kidney aggression. The impact of contrast administration on those biomarkers has not been specifically evaluated but could provide clues about the toxicity of contrast media. This study aimed at measuring changes in TIMP-2 and IGFBP-7 urinary concentrations before and after a contrast-enhanced computed tomography in critically ill patients.Methods77 patients were included in a prospective observational cohort study. Urinary [TIMP -2]·[IGFBP-7] was measured before, 6 and 24 h after contrast infusion. Urine output and serum creatinine were followed 3 days.ResultsMedian [TIMP-2]·[IGFBP-7] was 0.06 [interquartile range 0.04;0.26], 0.07 [0.03;0.34] and 0.10 [0.04;0.37] (ng/mL)2/1000 respectively before, 6 and 24 h after contrast infusion. Individual changes from baseline were − 0.01 [− 0.11;0.11] and 0.00 [− 0.10;0.09] (ng/ml)2/1000 at 6 and 24 h. These changes were not higher among the patients increasing their Kidney Disease Improving Global Outcome (KDIGO) classification within 3 days after contrast infusion (n = 14 [18%] based on creatinine criterion only, n = 42 [55%] based on creatinine and urine output).ConclusionsChanges in [TIMP-2]·[IGFBP-7] urinary concentration after contrast-enhanced computed tomography were insignificant, suggesting minimal kidney aggression by modern iodinated contrast media.
Highlights
Iodinated contrast media may contribute to acute kidney injury
To the best of our knowledge, the performance of [tissue inhibitor of metalloproteinase 2 (TIMP-2)]·[insulin like growth factor binding protein 7 (IGFBP-7)] has not been evaluated in toxic Acute kidney injury (AKI), despite some common pathophysiologic pathways shared among all AKI etiologies
Quantifying cell-cycle arrest biomarkers before and after iodinated contrast media (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 contrast-associated AKI (CA-AKI)
Summary
Iodinated contrast media may contribute to acute kidney injury. several recent works suggest that this toxicity is minimal in the clinical setting. Urinary G1 cell-cycle arrest proteins tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin like growth factor binding protein 7 (IGFBP-7) were identified as highly sensitive and specific biomarkers for early detection of kidney aggression. 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]. 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. In the clinical setting of multifactorial kidney aggression, evaluating the effect of iodinated CM on those biomarkers is important
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