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Renal Failure

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Risk of Acute Kidney Injury after Exposure to

Gadolinium-Based Contrast in Patients with Renal

Chih-Chiang Chien, Hsien-Yi Wang, Jhi-Joung Wang, Wei-Chih Kan, Tsair-Wei

Chien, Ching-Yih Lin & Shih-Bin Su

To cite this article: Chih-Chiang Chien, Hsien-Yi Wang, Jhi-Joung Wang, Wei-Chih Kan, Tsair-
Wei Chien, Ching-Yih Lin & Shih-Bin Su (2011) Risk of Acute Kidney Injury after Exposure to
Gadolinium-Based Contrast in Patients with Renal Impairment, Renal Failure, 33:8, 758-764, DOI:

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Published online: 22 Jul 2011.

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Renal Failure, 33(8): 758–764, (2011)
Copyright © Informa Healthcare USA, Inc.
ISSN 0886-022X print/1525-6049 online
DOI: 10.3109/0886022X.2011.599911


Risk of Acute Kidney Injury after Exposure to Gadolinium-Based

Contrast in Patients with Renal Impairment

Chih-Chiang Chien1,2 , Hsien-Yi Wang1 , Jhi-Joung Wang3 , Wei-Chih Kan1 , Tsair-Wei Chien4,5 ,
Ching-Yih Lin6 and Shih-Bin Su7,8
1 Department of Nephrology, Chi-Mei Medical Center, Tainan, Taiwan; 2 Department of Food Nutrition, Chung Hwa
University of Medical Technology, Tainan, Taiwan; 3 Department of Medical Research, Chi-Mei Medical Center, Tainan,
Taiwan; 4 Department of Management, Chi-Mei Medical Center, Tainan, Taiwan; 5 Department of Hospital and Health
Care Administration, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan; 6 Department of Internal Medicine,
Chi-Mei Medical Center, Tainan, Taiwan; 7 Department of Family Medicine, Chi-Mei Medical Center, Tainan, Taiwan;
8 Institute of Biomedical Engineering, Southern Taiwan University, Tainan, Taiwan

Objectives: Gadolinium-based contrast media (Gd-CM) are reported to induce acute kidney injury (AKI) in a high-risk
population group at the usual dose for magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA)
examinations. We assessed gadolinium-induced nephropathy in patients with renal impairment who underwent MRI
or MRA examinations, and evaluated the risk factors. Materials and methods: In this retrospective study, 238 patients
with baseline renal impairment, who received MRI or MRA examinations with Gd-CM, were recruited. After all other
AKI causes—liver decompensation, severe heart failure, all kinds of shock, and severe sepsis—and patients on dialysis
were excluded, 158 patients were enrolled. AKI was defined as a decrease in glomerular filtration rate (GFR) >10%
of baseline data within 3 days after administration of Gd-CM. Regression analysis was used to find independent risk
factors for gadolinium-induced AKI (Gd-AKI). Results: Twenty-six of the 158 patients (16.5%) developed Gd-AKI. There
were no significant differences in gender, age, or baseline GFR between those who did and who did not develop AKI.
Comorbid coronary artery disease, liver cirrhosis, diabetes mellitus, and hypertension were not significantly associated
with the development of Gd-AKI. However, sepsis was an independent risk factor for Gd-AKI after multivariate regres-
sion analysis (adjusted odds ratio: 4.417; 95% confidence interval: 1.671–11.676, p = 0.03). Conclusions: It is potential
AKI after administration of Gd-CM under sepsis condition at the dose for MRI and MRA examinations in patients with
renal impairment. It is important to identify high-risk patients and closely monitor renal function after administration of

Keywords: gadolinium-based contrast media, acute kidney injury, sepsis

INTRODUCTION risk of AKI with I-CM in patients with underly-

ing chronic renal impairment, intravenous gadolinium-
Contrast medium-induced nephropathy (CIN) is a
based contrast media (Gd-CM) have been widely used
serious complication of radiological examinations that
for magnetic resonance imaging (MRI) as an alternative
require iodinated contrast media (I-CM) enhancement
for diagnostic and interventional angiographic proce-
in high-risk patients.1 With increased diagnostic and
dures before the era of nephrogenic systemic fibrosis
therapeutic procedures requiring contrast medium, it
has been reported that CIN is the third most com-
Although it was thought to be safe and non-
mon cause of acute kidney injury (AKI) in hos-
nephrotoxic at the approved doses for MRI and
pitalized patients.2 Because of the well-documented

Chih-Chiang Chien and Hsien-Yi Wang contributed equally to this work.

Address correspondence to Shih-Bin Su, Department of Family Medicine, Chi-Mei Medical Center, 901 Jung-Hua Road, Yung Kang
City, Tainan 710, Taiwan. Tel.: +886-6-251-7844; Fax: +886-6-283-2639; E-mail:
Received 27 February 2011; Revised 25 May 2011; Accepted 15 June 2011

Acute Kidney Injury after Gadolinium-Based Contrast 759

magnetic resonance angiography (MRA) examinations The protocol of this study was approved by the
(≤0.3 mmol/kg),4 Gd-CM has recently been reported to Research and Ethics Review Board of Chi-Mei Medical
induce a reversible decrease of the glomerular filtration Center.
rate (GFR) in a high-risk group, especially in patients
with renal impairment.5–9 Additionally, patients usu- Statistical Analysis
ally have varied preexisting comorbidities [such as The data were analyzed using the Statistical Package
coronary artery disease (CAD), hypertension (HTN), for Social Sciences for Windows Version 17.0 (SPSS
diabetes, sepsis] when undergoing MRI or MRA exami- Inc., Chicago, IL, USA). A χ 2 test was used for non-
nations. However, additional studies have not confirmed numerical data. Regression analyses were done to find
whether these comorbid conditions are risk factors for independent variables for AKI. Significance was set at
Gd-induced nephropathy at low doses of Gd-CM. p < 0.05.
We hypothesized that Gd-CM is associated with AKI
in patients with baseline renal impairment and comor-
bidities. Therefore, the purpose of our study was to RESULTS
evaluate AKI after administration of Gd-CM in patients After excluding 80 patients by our exclusion crite-
with renal impairment who underwent MRI or MRA ria, 158 patients with impaired baseline renal function
examinations. Results were compared between patients were analyzed finally. Seventy-two (46%) were women
with and without AKI. Comorbid conditions and risk and 86 (54%) were men (Table 1). More than half
factors were also analyzed. of the patients were older than 65 years. Baseline
GFR was between 90 and 60 mL/min/1.73 m2 for 74
patients (46.8%), between 60 and 30 mL/min/1.73 m2
MATERIALS AND METHODS for 41 patients (25.9%), and below 30 mL/min/1.73
m2 for 43 patients (27.2%). Of the 158 patients,
Patients 58 patients (36.7%) had diabetes mellitus (DM), 66
We systematically reviewed the charts of 238 patients patients (41.8%) had HTN, and 65 patients (39.2%)
who underwent MRI or MRA examinations with Gd- had sepsis.
CM from January 2005 to December 2005. To be A decrease in GFR >25% below baseline data within
included, patients were required to have at least two 3 days after administration of Gd-CM was noted in
serum creatinine (sCre) values for a span of 7 or more only four patients (2.5%). However, there was no sig-
days before the MRI/MRA examinations and one sCre nificant difference between the number of patients with
value within 3 days after the examination. We selected and without GFR decline >25% based on gender, age,
patients whose renal function had been stable for 1 baseline GFR, and comorbidities (Tables 2 and 3).
week (definition: GFR change <10% during the week) We further analyzed the patient with a less stringent
before they were given Gd-CM. Impaired baseline renal criterion who had a decrease in GFR >10% below base-
function was defined as a pre-MRI/MRA examination line data within 3 days after administration of Gd-CM.
of GFR below 90 mL/min/1.73 m2 . The GFR value Twenty-six of the 158 patients (16.5%) developed GFR
was calculated using the Modification of Diet in Renal
Disease (MDRD) study equation.10
Table 1. Demographic characteristics of study patients at
Data Collection Female Male Total
n (%) n (%) n (%) p-Value
Patients who had been given any nephrotoxic agents
or other forms of contrast media (CM) within 4 weeks Age (years) 0.900
before the MRI/MRA examinations were excluded. We <51 12 (16.7) 16 (18.6) 28 (17.7)
51–65 18 (25.0) 25 (29.1) 43 (27.2)
also excluded patients with AKI with all other causes, 66–75 20 (27.8) 21 (24.4) 41 (25.9)
including liver decompensation, severe heart failure >75 22 (30.6) 24 (27.9) 46 (29.1)
(New York Heart Association Class III and IV), all kinds
of shock, and sepsis-related AKI, septic shock, severe Baseline eGFR (mL/min/1.73 m2 ) 0.070
90 > eGFR ≥ 60 30 (41.7) 44 (51.2) 74 (46.8)
sepsis,11 and patients on dialysis. 60 > eGFR ≥ 30 16 (22.2) 25 (29.1) 41 (25.9)
In this study, three kinds of intravenous contrast eGFR < 30 26 (36.1) 17 (19.8) 43 (27.2)
agents were used during MRI/MRA: Gd-DTPA (Mag-
Comorbid conditions
nevist, Schering AG, Berlin, Germany), Gd-DTPA- CAD 4 (5.6) 8 (9.3) 12 (7.6) 0.376
BMA (Omniscan, Amersham Health PLC, Carrigt- Liver cirrhosis 10 (13.9) 8 (9.3) 18 (11.4) 0.366
wohill, Ireland), and Gd-DO3A (Gadovist, Schering DM 31 (43.1) 27 (31.4) 58 (36.7) 0.130
AG, Berlin, Germany). The dose of Gd-CM for MRI HTN 29 (40.3) 37 (43.0) 66 (41.8) 0.727
or MRA examinations was 0.2 mmol/kg body weight in Sepsis 26 (36.1) 36 (41.9) 62 (39.2) 0.461
nearly all the patients. All patients received Gd-CM via Note: eGFR, estimated glomerular filtration rate; CAD, coro-
intravenous injection. nary artery disease; DM, diabetes mellitus; HTN, hypertension.

© 2011 Informa Healthcare USA, Inc.

760 C.-C. Chien et al.

Table 2. Associated factors and rapid decline in eGFR after administration of gadolinium-based contrast media
eGFR decline >25% eGFR decline >10%
p-Value p-Value
No (%) Yes (%) No (%) Yes (%)
Gender 0.857 0.715
Female 70 (97.2) 2 (2.8) 61 (84.7) 11 (15.3)
Male 84 (97.7) 2 (2.3) 71 (82.6) 15 (17.4)
Age (years) 0.613 0.668
<51 27 (96.4) 1 (3.6) 22 (78.6) 6 (21.4)
51–66 42 (97.7) 1 (2.3) 38 (88.4) 5 (11.6)
66–75 41 (100) 0 (0) 33 (80.5) 8 (19.5)
>75 44 (95.7) 2 (4.3) 39 (84.8) 7 (15.2)
Baseline eGFR (mL/min/1.73 m2 ) 0.751 0.686
90 > eGFR ≥ 60 72 (97.3) 2 (2.7) 61 (82.4) 13 (17.6)
60 > eGFR ≥ 30 40 (97.6) 1 (2.4) 36 (87.8) 5 (12.2)
eGFR < 30 42 (97.7) 1 (2.3) 35 (81.4) 8 (18.6)
Comorbid conditions
CAD 12 (100) 0 (0) 0.561 9 (75.0) 3 (25.0) 0.406
Liver cirrhosis 17 (94.4) 1 (5.6) 0.387 14 (77.8) 4 (22.2) 0.483
DM 58 (100) 0 (0) 0.123 50 (86.2) 8 (13.8) 0.492
HTN history 65 (98.5) 1 (1.5) 0.491 53 (80.3) 13 (19.7) 0.352
Sepsis 60 (96.8) 2 (3.2) 0.655 46 (74.2) 16 (25.8) 0.011∗
Notes: eGFR, estimated glomerular filtration rate; CAD, coronary artery disease; DM, diabetes mellitus; HTN,
∗ p < 0.05.

Table 3. Regression table showing significant independent variables for rapid decline in eGFR after administration of gadolinium-based
contrast media (Gd-CM).
eGFR decline >25% eGFR decline >10%
Univariate analysis Multivariate analysis Univariate analysis Multivariate analysis
Variable OR (95% CI) AOR (95% CI) OR (95% CI) AOR (95% CI)
Female 1 1 1 1
Male 0.833 (0.114–6.069) 0.413 (0.037–4.642) 1.45 (0.72–2.94) 0.99 (0.39–2.53)
Age (years)
<51 1 1 1 1
51–66 0.643 (0.039–10.717) 0.593 (0.027–13.162) 0.78 (0.31–1.99) 0.36 (0.09–1.49)
66–75 NA NA 0.94 (0.37–2.41) 0.70 (0.18–2.65)
>75 1.227 (0.106–14.191) 1.262 (0.082–19.476) 0.64 (0.24–1.71) 0.50 (0.13–1.90)
Baseline eGFR (mL/min/1.73 m2 )
90 > eGFR ≥ 60 1 1 1 1
60 > eGFR ≥ 30 0.900 (0.079–10.237) 1.279 (0.092–17.737) 0.65 (0.22–1.98) 0.50 (0.15–1.70)
eGFR < 30 0.857 (0.075–9.740) 1.187 (0.049–29.014) 1.07 (0.41–2.84) 0.85 (0.27–2.73)
No 1 1 1 1
Yes NA NA 1.02 (0.28–3.75) 2.12 (0.44–10.16)
Liver cirrhosis
No 1 1 1 1
Yes 2.686 (0.264–27.297) 5.026 (0.172–146.972 1.19 (0.37–3.81) 2.87 (0.69–11.89)
No 1 1 1 1
Yes NA NA 0.70 (0.33–1.49) 0.61 (0.22–1.69)
No 1 1 1 1
Yes 0.456 (0.046–4.487) 1.121 (0.079–15.866) 1.15 (0.57–2.30) 2.37 (0.9–6.17)
No 1 1 1 1
Yes 1.567 (0.215–11.421) 3.012 (0.235–38.556) 2.14 (1.07–4.28)∗ 4.42 (1.67–11.68)∗
Notes: eGFR, estimated glomerular filtration rate; OR, odds ratio; CI, confidence interval; AOR, adjusted odds ratio; CAD, coronary
artery disease; DM, diabetes mellitus; HTN, hypertension.
∗ p < 0.05.

Renal Failure
© 2011 Informa Healthcare USA, Inc.
Table 4. Gadolinium-based contrast-induced acute kidney injury (AKI) at dose ≤0.3 mmol/kg.
Baseline GFR/ Risk factor for
Author Number of patients Gd dose (mmol/kg) RR Comments
serum creatinine AKI
Robert et al.5 39 sCre = 2.11 mg/dL 0.15 Prospective observational study
One of 39 patients (3%) developed AKI after
angiography (definition of AKI: sCre
increase ≥0.5 mg/dL)
Sam et al.6 195 GFR = 38.2 ± 1.6 0.28 Renal Seven of 195 patients (3.5%) developed AKI
mL/min/1.73 m2 insufficiency after angiography (definition of AKI: sCre
in diabetes increase >1.0 mg/dL)
Ergün et al.8 91 GFR = 33 (15–58) 0.2 Diabetic 6.91 Retrospective study
mL/min/1.73 m2 nephropathy
Baseline GFR, 0.889 Eleven of 91 patients (12%) developed AKI
older age, after an MRI exam (definition of AKI:
anemia, sCre increase ≥0.5 mg/dL)
Retrospective study
This study 158 GFR = 52.1 ± 25.7 0.2 Sepsis 4.417 Twenty-six of 158 patients (16.5%)
mL/min/1.73 m2 developed AKI after an MRI exam
(definition of AKI: GFR decrease >10%)
Note: Gd, gadolinium; GFR, glomerular filtration rate; sCre, serum creatinine; RR, relative risk; MRI, magnetic resonance imaging.
Acute Kidney Injury after Gadolinium-Based Contrast 761
762 C.-C. Chien et al.

decline >10% after administration of Gd-CM. Comor- The risk of gadolinium-induced nephrotoxicity is
bid conditions with CAD, liver cirrhosis (LC), DM, and strongly demonstrated by some experimental studies.
HTN were not significantly associated with a decline in For example, when cultured renal tubular cells were
GFR after administration of Gd-CM (Table 2). How- incubated with Gd-CM and I-CM, the degree of cyto-
ever, 16 patients with sepsis (25.8%) had a rapid decline toxicity was similar.17 Nyman et al.19 report a signif-
in estimated glomerular filtration rate (eGFR). Patients icantly more pronounced decrease in GFR in animals
with sepsis had a higher risk for GFR decline after given Gd-CM than in those given I-CM.
administration of Gd-CM (p = 0.011). Although the risk factors for I-CM nephropathy are
Logistic regression analysis showed that sepsis was an well characterized, including renal impairment, diabetic
independent risk factor for GFR decline after adminis- nephropathy, congestive heart failure, volume depletion,
tration of Gd-CM (Table 3). GFR decline after admin- old age, high doses of CM simultaneously using nephro-
istration of Gd-CM was 3.417 times higher for patients toxic agents, and using a high osmolar contrast agent, 1
with sepsis than those without sepsis (95% confidence however, the risk factors for Gd-induced nephrotoxic-
interval: 1.67–11.68, p = 0.03). ity are not yet clear. Sam et al.6 showed that underlying
chronic renal impairment might be associated with Gd-
induced nephrotoxicity, and Ergün et al.8 reported that
lower GFR and diabetic nephropathy were independent
risk factors for AKI after exposure to Gd-GM. However,
In this study, we found that intravenous Gd-CM at we found it is potential AKI in GFR after administration
the dose for MRI and MRA examinations caused rapid of Gd-CM under sepsis condition.
GFR decline (defined as a decrease >10% in GFR) An increase in oxygen radical scavengers and a
in 16.5% of patients with preexisting renal impair- decrease in renal blood flow, which causes renal
ment. Age, gender, baseline GFR, DM, HTN, CAD, ischemia, have been proposed as the primary patho-
and LC were not associated with AKI after adminis- genetic sources of sepsis.11 The mechanism of
tration of Gd-CM. However, it is potential AKI after Gd-induced nephrotoxicity is not currently clearly
administration of Gd-CM under sepsis condition. understood. Gd-CM is hypertonic, has an osmolarity
DM, old age (>75 years old), heart failure, LC, 2–7 times greater than that of plasma, and is not
HTN, and lower baseline GFR are risk factors for absorbed by renal tubular epithelial cells. These charac-
I-CM nephropathy,1 but these risk factors for Gd-CM teristics of Gd chelates are similar to those of I-CM. The
nephropathy at the dose for MRI and MRA exam- injection of Gd-CM results in a substantial osmotic load
inations are controversial. This is because there are to the kidneys. High osmolar contrast media may induce
wide variations in definitions of AKI from one study to intense and prolonged vasoconstriction at the corti-
another (Table 4). AKI has been defined as an increase comedullary junction of the kidneys and directly impair
in sCre >0.3 mg/dL,12 >0.5 mg/dL,5,8,13 and >1 the autoregulatory ability of the kidney through a loss of
mg/dL.14 Additionally, outcome data based on comor- nitric oxide production.20–23 A sepsis-related decrease
bidities before MRI examinations were not reported in in renal blood flow and an increase in reactive oxygen
many studies.4 Tombach et al.14 reported that the use species expression may increase renal injury in patients
of Gd-CM at a dose of 0.3 mmol/kg in patients with given Gd-CM. Therefore, Gd-CM and sepsis appear
impaired renal function appeared not to be nephro- to synergistically interact in rapid GFR decline. If Gd-
toxic. Ergün et al.,8 however, found that AKI occurred CM is used in patients with sepsis, it will increase the
after Gd-CM in patients with preexisting stage 3 or incidence of GFR decline. We found that patients with
4 chronic kidney disease. Risk factors for gadolinium- sepsis but without evidence of AKI had a 3.417 times
induced AKI include diabetic nephropathy and low higher incidence of rapid GFR decline after exposure to
GFR. Gd-CM than did patients without sepsis.
Cases of CIN usually use the definition by a fixed A new and mysterious clinical–pathological entity
(0.5 mg/dL) or proportionate (25%) decline in GFR condition, NSF, has been described in patients with
levels after exposure to contrast media.1,5,8 However, severe renal failure within the past few years.24 Recent
sCre is not significantly changeable in early AKI, observations have linked NSF to using Gd-CM in these
because in the non-steady-state conditions of AKI, as renal-impaired patients.25 The Food and Drug Admin-
GFR falls, sCre secretion increases.15 In fact, histologi- istration has warned26 that physicians should carefully
cal data from a few animal studies suggest that Gd-CM assess the need for Gd-CM when doing an MRI or
induces acute tubular necrosis and cytoplasmic vac- MRA on patients with moderate to severe renal failure.
uolization in renal tubular cells in several hours.16–18 Our study has some limitations. First, it was ret-
For the above reasons, we further used a less stringent rospective. A retrospective study has a disadvantage
criterion (a decrease >10% in GFR) for AKI. This may to interpret this group of patients because numerous
explain why we found a higher incidence of AKI after variables can influence renal function. Second, it lacked
administration of Gd-CM at the doses for MRI and a control group. To show that Gd-CM is the cause of
MRA examinations. AKI, it is better to have a control group, although we

Renal Failure
Acute Kidney Injury after Gadolinium-Based Contrast 763

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tubular cells at angiographic concentrations: In vitro study.
This study was supported by grant CMFHR9951 from
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Renal Failure