Korean J Radiol. 2021 Sep;22(9):1547-1554. English.
Published online Jun 01, 2021.
Copyright © 2021 The Korean Society of Radiology
Original Article

Renal Safety of Repeated Intravascular Administrations of Iodinated or Gadolinium-Based Contrast Media within a Short Interval

Chiheon Kwon,1,* Koung Mi Kang,1,* Young Hun Choi,1 Roh-Eul Yoo,1 Chul-Ho Sohn,1 Seung Seok Han,2 and Soon Ho Yoon1
    • 1Department of Radiology, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea.
    • 2Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea.
Received September 22, 2020; Revised February 14, 2021; Accepted March 05, 2021.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective

We aimed to investigate whether repeated intravascular administration of iodinated contrast media (ICM) or gadolinium-based contrast agents (GBCAs) within a short interval was associated with an increased risk of post-contrast acute kidney injury (PC-AKI).

Materials and Methods

This retrospective study included 300 patients (mean age ± standard deviation, 68.5 ± 8.1 years; 131 male and 169 female) who had undergone at least one ICM-enhanced perfusion brain CT scan, had their baseline and follow-up serum creatinine levels available, and had not undergone additional contrast-enhanced examinations 72 hours before and after a time window of interest were included. The study population was divided into three groups: single-dose group and groups of patients who had received multiple contrast administrations in the time window of interest with the minimum contrast repeat interval either within 4 hours (0–4-hour group) or between 4 to 48 hours (4–48-hour group). Multivariable logistic regression analysis was conducted to evaluate the association between AKI and repeated ICM administrations. A similar supplementary analysis was performed including both ICM and GBCA.

Results

When ICM was only considered ignoring GBCA, among 300 patients, 207 patients received a single dose of ICM, 58 had repeated doses within 4 hours (0–4-hour group), and 35 patients had repeated doses between 4 to 48 hours (4–48-hour group). Most patients (> 95%) had a baseline estimated glomerular filtration rate (eGFR) of ≥ 30 mL/min/1.73 m2. AKI occurred in 7.2%, 13.8%, and 8.6% of patients in the single-dose, 0–4-hour, and 4–48-hour groups, respectively. In the 0–4-hour and 4–48-hour groups, additional exposure to ICM was not associated with AKI after adjusting for comorbidities and nephrotoxic drugs (all p values > 0.05).

Conclusion

Repeated intravascular administrations of ICM within a short interval did not increase the risk of AKI in our study patients suspected of acute stroke with a baseline eGFR of ≥ 30 mL/min/1.73 m2.

Keywords
Contrast media; Acute kidney injury; Retrospective studies; Tomography, X-ray computed; Magnetic resonance imaging

INTRODUCTION

Contrast media are indispensable in modern radiology, as they provide essential diagnostic information during CT and MR examinations. The use of iodinated contrast media (ICM) and gadolinium-based contrast agents (GBCAs) is generally considered safe, although adverse drug reactions, including hypersensitivity reactions and ICM-induced nephrotoxicity, are possible. Traditionally, post-contrast acute kidney injury (PC-AKI) has been recognized as one of the major causes of AKI in hospitalized patients, with an incidence of 0.6–30% [1, 2, 3]. However, recent well-designed studies and meta-analyses that adjusted for other risk factors have suggested that the nephrotoxicity of ICM is overestimated [4, 5, 6, 7].

Well-known risk factors for PC-AKI include impaired renal function, diabetes mellitus, cardiovascular disease, periprocedural hemodynamic instability, and nephrotoxic drugs [7, 8]. PC-AKI is also associated with the type and route of administration of ICM. In contrast with high-osmolar ICMs, low- to iso-osmolar ICMs are less nephrotoxic [9, 10, 11, 12]. Intra-arterial injections have been associated with a higher incidence of PC-AKI than intravenous administration [13]. Multiple doses of ICM within a short time interval have been proposed as another risk factor for PC-AKI [14].

Repeated ICM- or GBCA-enhanced examinations within a short interval are sometimes inevitable, particularly in emergent situations. For example, a patient with suspected acute or hyperacute stroke usually undergoes perfusion CT with CT angiography to determine intra-arterial thrombolysis, and intra-arterial thrombolysis also requires ICM administration, along with follow-up MR or CT examinations. A minimum dosing interval of 24 hours for repeated administrations of ICM has been suggested depending on the half-life of ICM [15]. With normal renal function, the half-life of ICMs is 1–2 hours; GBCAs have a similar half-life (1.3–1.6 hours). Therefore, most contrast media are eliminated before 24 hours [15, 16, 17, 18, 19, 20]. Currently, the American College of Radiology (ACR) guidelines do not specify a threshold. On the other hand, the European Society of Urogenital Radiology (ESUR) guidelines recommend ensuring at least a 4-hour interval between repeated exposures to ICM [15, 21]. Nevertheless, the renal safety of repeated exposure to ICM or GBCA within a short interval has rarely been investigated. Therefore, we aimed to investigate whether repeated intravascular administration of ICM or GBCA within a short interval was associated with an increased risk of AKI in patients recently exposed to ICM.

MATERIALS AND METHODS

This retrospective cohort study received Institutional Review Board approval, and the requirement for informed consent was waived (IRB No. 1802-015-919).

Study Population

We retrospectively searched the medical records of 692 consecutive patients suspected of acute stroke who underwent standardized ICM-enhanced perfusion brain CT from June 2015 to December 2017. As it was possible for patients to undergo multiple contrast-enhanced examinations before and after perfusion brain CT, we applied the following criteria to determine patient eligibility: 1) availability of baseline serum creatinine level before the first contrast-enhanced examination in the time window of interest (Fig. 1), 2) follow-up renal function tests within 72 hours after the last contrast-enhanced examination in the time window of interest (Fig. 1), and 3) satisfying the time-window criteria as shown in Figure 1.

Fig. 1
Time-window criteria.
The time window criteria in our study were defined as follows: 1) the time interval between the first and last contrast medium administrations was within 48 hours; 2) no other contrast medium study was performed within 72 hours before the first contrast medium administration; and 3) no other contrast medium study was performed 72 hours after the last contrast medium injection. The first and the last contrast medium administrations represent the same examination if the patient did not undergo repeat contrast injections (i.e., single dose). Minimum repeat interval applies only when the patient underwent multiple contrast injections in the time window of interest. It is defined as the shortest interval of any adjacent contrast medium injections. CE = contrast-enhanced

Eighty-five patients without baseline serum creatinine information were excluded, as well as 247 patients without follow-up renal function tests. A total of 300 patients (mean age ± standard deviation, 68.5 ± 8.1 years; 131 male and 169 female) were finally included in this study (Fig. 2). The patients were divided into three groups according to the ‘minimum repeat interval’ as shown in Figure 1: single-dose group (i.e., no repeat exam), 0–4-hour group (i.e., minimum repeat interval less than 4 hours), and 4–48-hour group (minimum repeat interval of 4 to 48 hours) (Fig. 2). As renal safety issues mostly arise with the use of ICMs, our study primarily focused on the analysis of repeat administrations of ICM. However, we have also performed additional analysis considering both ICM and GBCA.

Fig. 2
Flow diagram for the study design.
The patient numbers for single-dose group, 0–4-hour group, and 4–48-hour group are according to the administrations of iodinated contrast media alone, ignoring gadolinium-based contrast agent.

CT and MR Examinations

At our institution, iomeprol is routinely used for perfusion brain CT scans, making it the most common intravenous ICM used in this study group. Other ICMs, including iohexol, ioversol, iopamidol, and iobitridol, were also administered for scans of other body parts or in patients with a history of hypersensitivity to iomeprol. For intra-arterial ICM, however, iopamidol was primarily administered, and ioversol and iobitridol were administered in exceptional cases similar to those that necessitated the use of other intravenous ICMs. We reviewed the type and volume of ICM administered for each CT examination.

Most of the MR examinations were for the brain, except the few cases for the abdominal, pelvic, and musculoskeletal areas. Either gadoterate meglumine or gadobutrol were used for contrast-enhanced MR studies. Contrast-enhanced T1-weighted MR imaging was performed after the intravenous administration of GBCA at a dose of 0.1 mmoL/kg of body weight.

Investigated Variables

Demographic information (age, sex, and body mass index), type and route of contrast medium administration (intravenous ICM, intra-arterial ICM, and GBCA), and serum creatinine levels were extracted from the electronic medical records. In addition, patient comorbidities (myocardial infarction, chronic heart failure, peripheral vessel disease, chronic pulmonary disease, dementia, peptic ulcer, rheumatoid disease, cerebrovascular disease, paralysis, diabetes mellitus, chronic kidney disease, cancer, liver disease, and AIDS), recent history of potentially nephrotoxic medication (antibiotics, vancomycin, angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, chemotherapeutic drugs, COX-2 inhibitors, loop diuretics, hydrochlorothiazide, immunosuppressant agents, sirolimus, nonsteroidal anti-inflammatory drugs [NSAIDs], and statins), and the use of N-acetylcysteine as a preventive measure were assessed. We calculated the Charlson comorbidity index [22, 23].

Definition of AKI

The definition of PC-AKI is quite different from that of AKI, although there is no solid basis for this discrepancy, as pointed out in the Acute Kidney Injury Network guideline [24]. For consistency with previous studies on PC-AKI, we defined AKI as an increase in serum creatinine by 0.3 mg/dL or 25% above the baseline value within 72 hours without an alternative etiology; this is a widely accepted definition of PC-AKI [7, 20, 25]. In patients who underwent multiple contrast-enhanced examinations, the occurrence of AKI was observed within the time window from the first exposure to contrast medium to 72 hours after the last exposure to contrast medium.

Statistical Analysis

The Mann-Whitney U test (continuous variables) or the Fisher's exact test (categorical variables) was used for univariable analyses, and variables with p values less than 0.1 were selected as potential confounding factors in the subsequent multivariable logistic regression analysis conducted to examine the association between repeated contrast medium administration (independent variable) and PC-AKI (dependent variable). The odds ratio (OR) for the 0–4 and 4–48 groups was calculated considering the single-dose group as the reference. Statistical analysis was performed using SPSS version 25 (IBM Corp.).

RESULTS

Baseline Characteristics

In our study population, 47.3% of the patients had at least one additional contrast medium administration within 48 hours (Table 1). Ninety-three patients (31.0%) had additional administration of intravenous or intra-arterial ICM, while 79 patients (26.3%) underwent GBCA-enhanced MRI examination. When only ICM administrations were counted, 207 (69.0%), 58 (19.3%), and 35 (11.7%) patients were classified into the single-dose group, 0–4-hour group, and 4–48-hour group, respectively (Table 2). The mean amount ± standard deviation of ICM used was 147.2 ± 139.9 mL, and the mean volume ± standard deviation of intravenous administrations of GBCA was 6.1 ± 1.2 mL.

Table 1
Distribution of the Number of Repeated Contrast Medium Administrations within 48 Hours

Table 2
Comparison between Single and Multiple Iodinated Contrast Medium Administrations

AKI and Baseline Renal Functions

When ICM administration was only considered, AKI occurred in 15 of 207 patients (7.2%; 95% confidence interval [CI], 3.7% to 10.8%) in the single-dose group, 8 of 58 patients (13.8%; 95% CI, 4.9% to 22.7% in the 0–4-hour group, and 3 of 35 patients (8.6%; 95% CI, 0% to 17.8%) in the 4–48-hour group (Table 2). The mean baseline estimated glomerular filtration rates (eGFRs) ± standard deviation were 80.1 ± 29.2, 75.7 ± 18.5, and 70.5 ± 51.6 mL/min/1.73 m2 in the single-dose, 0–4-hour, and 4–48-hour groups, respectively (Table 2).

Association between AKI and Repeated Exposure to Contrast Medium

Univariable analyses found no significant difference in the incidence of AKI following the single and multiple ICM administrations (p = 0.783 and p = 0.454 for 0–4-hour and 4–48-hour groups, respectively). In the univariable analyses, baseline eGFR (p = 0.017), myocardial infarction (p = 0.013), congestive heart failure (p = 0.024), diabetes mellitus (p = 0.046), cancer (p = 0.084), and the use of antibiotics (p = 0.003), loop diuretics (p = 0.001), NSAIDs (p = 0.021), and statins (p = 0.062) were selected as potential confounding factors in the subsequent multivariable logistic regression analysis (Table 2). Finally, the multivariable analysis showed the absence of a significant association between repeated contrast medium injections and the occurrence of PC-AKI (p = 0.147, OR = 2.217, 95% CI for OR: 0.756, 6.504 for 0–4-hour group; and p = 0.570, OR = 0.644, 95% CI for OR: 0.141–2.943 for the 4–48-hour group) (Table 3). In addition, when the analysis was extended with considerations of both ICM and GBCA, repeated contrast medium administration within a short interval did not increase the risk of PC-AKI (Table 4).

Table 3
Multivariable Analyses for the Association between Acute Kidney Injury and Repeated Exposures to Iodinated Contrast Medium

Table 4
Multivariable Analyses for the Association between Acute Kidney Injury and Repeated Exposures to Iodinated Contrast Medium or Gadolinium-Based Contrast Agent

DISCUSSION

PC-AKI has long been a concern in radiology, although some recent reviews have questioned the causal association between ICM and AKI [5]. The renal safety of shortly repeated ICM injections has not been investigated much, and previous reports on this issue have demonstrated controversial results [26, 27, 28, 29, 30, 31, 32, 33]. Furthermore, conflicting evidence exists on the renal safety of GBCAs [34], and the mixed use of ICMs and GBCAs within a short interval remains unclear.

The primary pathophysiological pathway of PC-AKI involves impaired renal perfusion. Complex mediators triggered by ICM cause hypoxic damage to the renal medulla, which leads to acute tubular necrosis [35]. GBCAs, despite having entirely different chemical structures, share similar characteristics with ICM, including hypertonicity and renal clearance properties. It can be inferred that the pathophysiology of the nephrotoxicity of GBCAs may be similar to that of the nephrotoxicity of ICMs [34], as renal glomerular filtration is almost the exclusive mechanism underlying GBCA elimination [19, 34]. Additionally, the release of free gadolinium ions in patients with decreased renal function may be another cause of nephrotoxicity [34, 36].

It has been conventionally suggested that patients who have recently been exposed to ICM wait for 24 hours for the next dose. As ICMs and GBCAs have a half-life shorter than 2 hours, only 25% are left after 4 hours, and these agents are almost eliminated after 24 hours. The ACR guideline points out this ambiguity; therefore, it does not endorse a specific time interval or threshold volume for an additional contrast medium [15]. In the ESUR guidelines, different dosing intervals for different contrast media are suggested, as follows: 1) between two ICM injections: 4 hours in patients with a GFR > 30 mL/min/1.73 m2 and 48 hours in patients with a GFR of < 30 mL/min/1.73 m2; 2) between two GBCA injections: 4 hours in patients with a GFR of > 30 mL/min/1.73 m2 and 7 days in patients with a GFR of < 30 mL/min/1.73 m2; 3) between ICM and GBCA injections: 4 hours in patients with a GFR of > 30 mL/min/1.73 m2 and 7 days for patients with a GFR of < 30 mL/min/1.73 m2 [21].

Our study sheds light on this ambiguity. In the general population, analyzing this issue is challenging because repeated contrast medium administration within a short time interval is uncommon, except for emergent situations. In patients suspected of an acute or hyperacute stroke, however, GBCA, intravenous ICM, and intra-arterial ICM are frequently administered shortly after each other within a limited time window. When neurological symptoms are at stake, a short dosing interval is recommended due to the temporal urgency of the situation, as is well-emphasized by “time is brain” [37]. With that in mind, we limited the study population to patients who underwent perfusion brain CT.

Additional exposure to ICM or GBCA within a short interval was not associated with AKI in this population, which mostly had a GFR of > 30 mL/min/1.73 m2. In line with this, concerns about the total volume of ICMs within a short interval can be addressed. Repeated administration of contrast medium at short intervals can increase the volume of the contrast medium in the body. The risk of PC-AKI increased with larger volumes of intra-arterial ICM with a single injection, whereas the volume of intravenously injected ICM has not been reported to be an independent risk factor for PC-AKI [38]. The volume of ICM to be administered via intra-arterial injection was recommended to be below 100 mL in patients with an eGFR < 60 mL/min/1.73 m2 [39]. In our population, the total volume of contrast medium was generally 150 mL or less, while the volume of intra-arterial ICM was generally 60 mL or less. In addition, when analyzed as an independent variable, the volume of ICM demonstrated no statistical correlation with the risk of PC-AKI (p = 0.080), which was omitted from our multivariable logistic regression model to avoid collinearity. The lack of an association between repeated exposure to contrast medium and AKI may be attributed to the relatively small volume of ICM (both total and intra-arterial) administered in this population.

Interestingly, even an additional exposure to ICM or GBCA within 4 hours did not increase the risk of AKI beyond the recommendations of the ESUR guidelines, although the baseline eGFR should be considered. In this study, approximately three-quarters of the study population had a baseline eGFR of 60 mL/min/1.73 m2 or higher. The number of patients with a baseline eGFR between 30 and 60 mL/min/1.73 m2 was relatively small. Considering the distribution of the baseline eGFR values, our results may not be interpreted as fully confirming the safety of repeated ICM administration, particularly for patients with a baseline eGFR between 30 and 60 mL/min/1.73 m2 who are potentially vulnerable to PC-AKI. Further studies with a well-organized cohort or randomized studies are warranted.

AKI occurred in 8.7% of patients in our study, which is a higher proportion than those reported in recent studies that used a single dose of contrast medium [4, 7]. The higher proportion is attributable to the older age and more comorbidities in our study group than in the general population. Furthermore, the study population mostly comprised hospitalized patients since the inclusion criteria required follow-up renal function testing. The use of complex medications for managing stroke and underlying comorbidities may also have contributed to the high frequency of AKI.

Our study had several other limitations. First, this study analyzed a single-center retrospective cohort with a relatively small sample size. Second, a considerable proportion of the cohort population was excluded because of a lack of baseline or follow-up serum creatinine levels. Third, since it was not feasible to measure the exact concentrations of contrast medium used for the interventional radiological procedures, rough estimations were made based on the billing records, and the dose of contrast medium used was accounted in units of bottles (50 cc). Fourth, we could not quantitatively analyze intravenous hydration, which may be protective against AKI. Fifth, our results cannot exclude the possibility of subclinical nephrotoxicity from the repeated administration of contrast media due to a lack of diagnostic tools for detecting subclinical nephrotoxicity [40].

In conclusion, repeated exposure to iodinated or GBCA within a short interval did not increase the risk of AKI in our study patients suspected of acute stroke with a baseline eGFR of 30 mL/min/1.73 m2 or higher.

Notes

Conflicts of Interest:The authors have no potential conflicts of interest to disclose.

Author Contributions:

  • Conceptualization: Soon Ho Yoon, Koung Mi Kang.

  • Data curation: Chiheon Kwon, Koung Mi Kang.

  • Formal analysis: Chiheon Kwon, Koung Mi Kang, Soon Ho Yoon.

  • Investigation: Chiheon Kwon, Koung Mi Kang, Roh-Eul Yoo, Chul-Ho Sohn.

  • Methodology: Chiheon Kwon, Soon Ho Yoon, Young Hun Choi, Seung Seok Han.

  • Resources: Soon Ho Yoon, Koung Mi Kang.

  • Supervision: Soon Ho Yoon.

  • Writing—original draft: Chiheon Kwon.

  • Writing—review & editing: Chiheon Kwon, Soon Ho Yoon, Koung Mi Kang.

Acknowledgments

The authors would like to acknowledge Andrew Dombrowski, PhD (Compecs, Inc.) for his assistance in improving the use of English in this manuscript.

References

    1. Finn WF. The clinical and renal consequences of contrast-induced nephropathy. Nephrol Dial Transplant 2006;21:i2–i10.
    1. Lasser EC, Lyon SG, Berry CC. Reports on contrast media reactions: analysis of data from reports to the U.S. Food and Drug Administration. Radiology 1997;203:605–610.
    1. Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int Suppl 2006;69:S11–S15.
    1. McDonald JS, McDonald RJ, Comin J, Williamson EE, Katzberg RW, Murad MH, et al. Frequency of acute kidney injury following intravenous contrast medium administration: a systematic review and meta-analysis. Radiology 2013;267:119–128.
    1. McDonald RJ, McDonald JS, Bida JP, Carter RE, Fleming CJ, Misra S, et al. Intravenous contrast material-induced nephropathy: causal or coincident phenomenon? Radiology 2013;267:106–118.
    1. McDonald JS, McDonald RJ, Williamson EE, Kallmes DF. Is intravenous administration of iodixanol associated with increased risk of acute kidney injury, dialysis, or mortality? A propensity score-adjusted study. Radiology 2017;285:414–424.
    1. Moos SI, van Vemde DN, Stoker J, Bipat S. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol 2013;82:e387–e399.
    1. McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F, et al. Risk prediction of contrast-induced nephropathy. Am J Cardiol 2006;98:27K–36K.
    1. Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993;188:171–178.
    1. Eng J, Wilson RF, Subramaniam RM, Zhang A, Suarez-Cuervo C, Turban S, et al. Comparative effect of contrast media type on the incidence of contrast-induced nephropathy: a systematic review and meta-analysis. Ann Intern Med 2016;164:417–424.
    1. Heinrich MC, Häberle L, Müller V, Bautz W, Uder M. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: meta-analysis of randomized controlled trials. Radiology 2009;250:68–86.
    1. Nielsen YW, Thomsen HS. Current evidence of contrast medium-induced nephropathy (CIN) after administration of low-osmolarity iodine-based contrast agents. Curr Radiol Rep 2017;5:52
    1. Schönenberger E, Martus P, Bosserdt M, Zimmermann E, Tauber R, Laule M, et al. Kidney injury after intravenous versus intra-arterial contrast agent in patients suspected of having coronary artery disease: a randomized trial. Radiology 2019;292:664–672.
    1. Gleeson TG, Bulugahapitiya S. Contrast-induced nephropathy. AJR Am J Roentgenol 2004;183:1673–1689.
    1. American College of Radiology. Manual on contrast media. Version 2021. Acr.org Web site. [Accessed Feburary 12, 2021].
    1. Bellin MF. MR contrast agents, the old and the new. Eur J Radiol 2006;60:314–323.
    1. Katzberg RW. Urography into the 21st century: new contrast media, renal handling, imaging characteristics, and nephrotoxicity. Radiology 1997;204:297–312.
    1. Krause W, Schuhmann-Giampieri G, Staks T, Kaufmann J. Dose proportionality of iopromide pharmacokinetics and tolerability after i.v. injection in healthy volunteers. Eur J Clin Pharmacol 1994;46:339–343.
    1. Perazella MA. Current status of gadolinium toxicity in patients with kidney disease. Clin J Am Soc Nephrol 2009;4:461–469.
    1. Thomsen HS, Morcos SK. Contrast media and the kidney: European Society of Urogenital Radiology (ESUR) guidelines. Br J Radiol 2003;76:513–518.
    1. European Society of Urogenital Radiology. ESUR guidelines on contrast media. Version 10.0. Esur.org Web site. [Accessed Feburary 12, 2021].
    1. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis 1987;40:373–383.
    1. Quan H, Li B, Couris CM, Fushimi K, Graham P, Hider P, et al. Updating and validating the Charlson comorbidity index and score for risk adjustment in hospital discharge abstracts using data from 6 countries. Am J Epidemiol 2011;173:676–682.
    1. KDIGO AKI Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2012;2:1–138.
    1. Morcos SK, Thomsen HS, Webb JA. Contrast-media-induced nephrotoxicity: a consensus report. Eur Radiol 1999;9:1602–1613.
    1. Balemans CE, Reichert LJ, van Schelven BI, van den Brand JA, Wetzels JF. Epidemiology of contrast material-induced nephropathy in the era of hydration. Radiology 2012;263:706–713.
    1. van der Molen AJ, Reimer P, Dekkers IA, Bongartz G, Bellin MF, Bertolotto M, et al. Post-contrast acute kidney injury - Part 1: definition, clinical features, incidence, role of contrast medium and risk factors: recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol 2018;28:2845–2855.
    1. Isaka Y, Hayashi H, Aonuma K, Horio M, Terada Y, Doi K, et al. Guideline on the use of iodinated contrast media in patients with kidney disease 2018. Circ J 2019;83:2572–2607.
    1. Trivedi H, Foley WD. Contrast-induced nephropathy after a second contrast exposure. Ren Fail 2010;32:796–801.
    1. Hong SI, Ahn S, Lee YS, Kim WY, Lim KS, Lee JH, et al. Contrast-induced nephropathy in patients with active cancer undergoing contrast-enhanced computed tomography. Support Care Cancer 2016;24:1011–1017.
    1. Hopyan JJ, Gladstone DJ, Mallia G, Schiff J, Fox AJ, Symons SP, et al. Renal safety of CT angiography and perfusion imaging in the emergency evaluation of acute stroke. AJNR Am J Neuroradiol 2008;29:1826–1830.
    1. Oleinik A, Romero JM, Schwab K, Lev MH, Jhawar N, Delgado Almandoz JE, et al. CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy. Stroke 2009;40:2393–2397.
    1. Langner S, Stumpe S, Kirsch M, Petrik M, Hosten N. No increased risk for contrast-induced nephropathy after multiple CT perfusion studies of the brain with a nonionic, dimeric, iso-osmolal contrast medium. AJNR Am J Neuroradiol 2008;29:1525–1529.
    1. Ledneva E, Karie S, Launay-Vacher V, Janus N, Deray G. Renal safety of gadolinium-based contrast media in patients with chronic renal insufficiency. Radiology 2009;250:618–628.
    1. Wong PC, Li Z, Guo J, Zhang A. Pathophysiology of contrast-induced nephropathy. Int J Cardiol 2012;158:186–192.
    1. Port M, Idée JM, Medina C, Robic C, Sabatou M, Corot C. Efficiency, thermodynamic and kinetic stability of marketed gadolinium chelates and their possible clinical consequences: a critical review. Biometals 2008;21:469–490.
    1. Gomez CR. Editorial: time is brain!. J Stroke Cerebrovasc Dis 1993;3:1–2.
    1. Bae KT. Intravenous contrast medium administration and scan timing at CT: considerations and approaches. Radiology 2010;256:32–61.
    1. Davidson C, Stacul F, McCullough PA, Tumlin J, Adam A, Lameire N, et al. Contrast medium use. Am J Cardiol 2006;98:42K–58K.
    1. Davenport MS, Cohan RH, Khalatbari S, Ellis JH. The challenges in assessing contrast-induced nephropathy: where are we now? AJR Am J Roentgenol 2014;202:784–789.

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