BJA Education, 20(12): 417e423 (2020)

doi: 10.1016/j.bjae.2020.07.006
Advance Access Publication Date: 3 October 2020

Matrix codes: 1A02,

2A05, 3I00

Contrast-associated acute kidney injury

M. Everson1,*, K. Sukcharoen2 and Q. Milner2
1
University Hospitals Plymouth NHS Trust, Plymouth, UK and 2Royal Devon & Exeter NHS Foundation
Trust, Exeter, UK
*Corresponding author: matthew.everson@nhs.net

Keywords: acute kidney injury; chronic kidney disease; contrast agent

Learning objectives Key points

By reading this article you should be able to:

Discuss the current evidence for the association
between contrast administration and develop-
ment of AKI.

Identify patients at high risk of developing CA-
AKI.

Implement preventative measures to reduce the
risk of CA-AKI.
Acute kidney injury (AKI) is common, occurring in more than
15% of patients admitted to hospital as an emergency.1 AKI
often indicates severe systemic dysfunction and can lead to
chronic kidney disease (CKD) and increased mortality. Early
proactive recognition, prevention and active management can
reduce the incidence of AKI.
Contrast-associated AKI (CA-AKI) is typified by a deterio-
ration of renal function in the days after intravascular injec-
tion of a contrast agent. Historically, the prevalence of CA-AKI
was thought to be substantial, and considered to be a direct
effect of iodinated contrast agents. Newer evidence questions
the prevalence of CA-AKI and the significance of contrast in
contributing towards AKI.2 In this review we describe the
Matthew Everson BSc (Hons) MRCP FRCA is a specialty registrar in
intensive care medicine and anaesthesia in the South West Peninsula
Deanery. His interests are in perioperative medicine, vascular
anaesthesia and medical education.
Kittiya Sukcharoen MRCP is an academic clinical fellow and spe-
cialty registrar in renal and general medicine in the South West
Peninsula. She has research interests in monogenic renal disease and
big data analysis.

Exposure to a contrast agent is associated with
acute kidney injury (CA-AKI) and the cause is
likely to be multifactorial.

Risk factors for CA-AKI include chronic kidney
disease (CKD), old age and hypovolaemia.

Alternative imaging techniques should be
considered for patients at high risk of CA-AKI.

Expansion of intravascular volume and using
lower osmolality contrast agents reduce the risk
of CA-AKI.
pathophysiological mechanisms and discuss the difference
between contrast-induced AKI (CI-AKI) and CA-AKI; research
data have not yet clearly distinguished these entities.
Regardless of aetiology, AKI can occur after giving an intra-
vascular contrast agent. We discuss how to identify those
patients at high risk of CA-AKI and the evidence-based pre-
ventative measures that should be taken to reduce the risk.
History and discovery of CA-AKI
CA-AKI was first described in the 1950s in patients undergoing
intravenous (i.v.) pyelography using contrast agents.3 Larger
studies that followed showed a very high incidence of CA-AKI.
It became widely believed that CA-AKI was associated with
substantially increased mortality and morbidity, including the
frequent need for renal replacement therapy (RRT). Unfortu-
nately, many of these early studies did not include control
groups, therefore only demonstrated association with and not
causation of the AKI. A meta-analysis examining the inci-
dence of CA-AKI after an i.v. contrast agent found that only 13
studies of 1489 papers had suitable control groups.2

Quentin Milner FRCA is a consultant anaesthetist with specialist

interest in vascular anaesthesia.

Accepted: 20 July 2020

© 2020 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
For Permissions, please email: permissions@elsevier.com

417
Acute kidney injury

Definition
Table 1 Risks factors for CA-AKI1,4
CI-AKI is the subgroup of CA-AKI that can be linked causally to
giving contrast media (i.e. ‘contrast-induced’). ‘Contrast- 1
Patient Pre-existing renal eGFR<60 ml min
induced nephropathy’ was a historic definition, replaced by factors disease (CKD or recent 1.73 2
CI-AKI, the term endorsed by Kidney Disease: Improving AKI)
Global Outcomes (KDIGO).4 The differences between CI-AKI Elderly population >75 yr
Diabetes Especially with
and CA-AKI have become blurred in the literature. This
associated renal
makes accurate reporting of the prevalence of CA-AKI prob- disease (eGFR<40 ml
lematic and has led to publication of poor quality data on the min1 1.732)
risk factors, prevention and treatments. KDIGO defines CI- Cardiovascular disease Cardiac failure,
AKI, after exposure of a contrast agent, as one of the following: hypertension or
vascular disease
(i) an increase in serum creatinine by 26.5 mmol L1 within Concurrent Including
48 h; or nephrotoxic drugs aminoglycosides,
(ii) an increase in serum creatinine by 1.5-fold from base- NSAID, antiviral drugs
(e.g. acyclovir)
line within 1 week; or
Haemodynamic Including
(iii) urine output <0.5 ml kg1 h1 of body weight for >6 instability hypovolaemia and
consecutive hours. sepsis. Where possible,
administration of
The creatinine definition is the most sensitive, but its
contrast should be
specificity is poor. delayed until
Without appropriate randomised trials, it is impossible to hypotension is
attribute AKI after contrast to be specifically contrast-induced. corrected. Intervention
We have therefore used the more inclusive term CA-AKI in or scanning with
this article. We believe what much of the literature describes contrast, however,
should not wait for
as CI-AKI is most likely to be CA-AKI. As one example, a study
renal function
by Ho and Harahsheh stated that 41% of 137 patients under- assessment if early
going computed tomography pulmonary angiography (CTPA) imaging outweighs the
developed CI-AKI, with 26% requiring RRT.5 However, 51% of risk of delaying the
the cohort were hypotensive, 39% required inotropic drugs procedure
and 50% received mechanical ventilation; this demonstrates Procedural Intra-arterial delivery, The risk is highest with
factors compared with the first-pass renal arterial
how various causes of AKI have been attributed solely to
lower risk of i.v. exposure, for example
contrast. delivery injection into the left
CA-AKI typically occurs within 48 h of receiving contrast heart, thoracic aorta,
with recovery expected, in most cases, over the next 5 days. suprarenal abdominal
Other causes of AKI, such as hypotension, embolic disease aorta or renal arteries
and medications should be considered, investigated and Contrast Dose of contrast High volumes of
managed as necessary. factors iodinated contrast
Estimated glomerular filtration rate (eGFR) and creatinine >350 ml or >4 ml kg1
clearance are widely used to describe renal function in stable High-osmolality
contrast
patients, but are unreliable in patients with acute illness,
Repeated exposure to Especially <72 h
when creatinine is preferred. contrast

Pathophysiology
The pathophysiological mechanisms of CA-AKI are not
completely understood. Contrast agents are thought to have
both direct and indirect effects on renal function. Contrast is
directly nephrotoxic to renal tubular cells by increasing
tubular fluid viscosity, leading to changes in renal tubular cell
polarity via redistribution of Naþ/Kþ ATPase pump expres-
sion, resulting in increased sodium delivery to the distal tu-
bules. This causes endothelial cell apoptosis, necrosis and
luminal obstruction, increased intratubular pressure and ul-
timately decreased glomerular filtration.
The indirect effect of contrast agents results in alterations
to vasoactive substances, such as renin, angiotensin, endo-
thelin, nitric oxide and prostaglandins. This causes reduced
glomerular blood flow and oxygen delivery to the metaboli-
cally active nephron. Contrast also increases blood osmolality
and viscosity. Collectively, these mechanisms, especially in
vulnerable renal tissues, can lead to impaired renal function.
Attributing AKI after a contrast agent solely to these
mechanisms is unproved. Non-contrast mediated mecha-
nisms also are at play. These include, for example, concurrent
haemodynamic instability, dehydration, other nephrotoxic
agents, the pathology for which the contrast agent is being
given and a patient’s comorbidities.
Types of contrast
Contrast is used to enhance tissue visibility, improve diag-
nostic efficacy or make therapeutic procedures possible. CA-
AKI is associated with giving an iodinated contrast agent.

418 BJA Education - Volume 20, Number 12, 2020


However, non-iodinated contrast agents, including
gadolinium-based contrast agents (GBCAs), may also induce
AKI (discussed later).
High osmolality contrast agents, used historically, have
approximately four times the osmolality of blood. These have
been largely replaced with either low osmolality agents,
which are still hyperosmolar (approximately 600 mOsm kg1),
with an osmolality twice that of blood (serum 290 mOsm
kg1), or iso-osmolar agents.
A randomised trial demonstrated a 3.3 times greater risk of
developing AKI in those receiving a high osmolality contrast
agent (diatrizoate, >1550 mOsm kg1) compared with a lower
osmolality agent (iohexol, <844 mOsm kg1).6 High osmolality
contrast agents have been predominantly abandoned by
radiological departments in the UK and the use of iso-osmolar
and low-osmolar agents is recommended by the European
Society of Cardiology, as these carry a lower risk of CA-AKI.7
Study heterogeneity makes it difficult to ascertain the
different incidence of AKI between iso-osmolar and low-
osmolar contrast agents, but they are lower than high-
osmolar agents. The randomised, double blind Cardiac Angi-
ography in Renally Impaired Patients (CARE) trial directly
compared iso-osmolar and low-osmolar contrast agents in
those with CKD undergoing percutaneous coronary inter-
vention (GFR 20e59 ml min1 1.732).8 The incidence of AKI
after intra-arterial contrast in both groups was not signifi-
cantly different (4.4% in the low-osmolarity group compared
with 6.7% in the iso-osmolarity group, p¼0.39), though the
mean increase in serum creatinine was lower in those
receiving low-osmolarity contrast.
Risk factors
The risk of developing CA-AKI depends on factors related to
the patient, the procedure and the type of contrast (Table 1).
Pre-existing renal dysfunction is the greatest patient-
related risk factor for CA-AKI. Those patients with a normal
baseline renal function have an estimated 1e2% risk of
developing CA-AKI.4 The risk of CA-AKI is 5% in those with a
pre-existing eGFR60 ml min1 1.732; 10% at eGFR 45e59 ml
min1 1.732; 15% at eGFR 30e44 ml min1 1.732; and 30% at
eGFR<30 ml min1 1.732.
The risk of CA-AKI with i.v. contrast for CT scans is low. A
large meta-analysis showed no increased risk of CA-AKI with
i.v. contrast compared with non-contrast CT scans; there were
similar incidences of AKI (6.4% contrast vs 6.5% non-contrast),
death or dialysis in both groups.2 However, this risk is likely to
be increased in the patient who is critically unwell and those
with other risk factors.
Patients who are given arterial contrast, compared with
i.v., are a different group of patients, receive different doses of
contrast and often experience procedure-related physiolog-
ical changes, such as hypotension and arterial embolisation.
Controlled studies comparing intra-arterial and i.v. contrast
agents are not feasible, as the contrast is essential for arterial
procedures.
Risk stratification tools, derived from large groups of pa-
tients, help to identify those at low or high risk of CA-AKI.
Those deemed low risk can avoid unnecessary renal func-
tion tests or overburdensome preventative measures; patients
at high risk can receive preventative measures with close
follow-up, with the aim of reducing the occurrence of CA-AKI.
Cumulative risk factors increase the possibility of developing
AKI exponentially.4 Most of these risk tools are developed for
Acute kidney injury
cardiac interventions. One such tool, published by Mehran
and colleagues, based on patients undergoing coronary in-
terventions, can be seen in Tables 2 and 3.9 We are not aware
of a risk score available for patients receiving i.v. contrast.
Prognosis
In most patients, CA-AKI is transient and self-limiting, but for
some it can lead to the development of de novo CKD or pro-
gression of pre-existing CKD.4 There are limited data in pa-
tients with end-stage renal failure on the development of CA-
AKI. In early studies, RRT for CA-AKI was used in almost 4% in
those with CKD.10 More recent studies provide a more relevant
risk, demonstrating an incidence of CA-AKI of around 5% and
only a small proportion of these patients go on to develop CKD
(1%) or require long-term RRT (0.06%) with i.v. contrast.11
Multiple studies demonstrate that CA-AKI is associated
with increased mortality, prolonged duration of hospital stay
and other adverse outcomes, even mild significant deteriora-
tion in renal function that is not clinically significant. A US
retrospective analysis of 27,608 patients undergoing percuta-
neous coronary intervention showed that even a small in-
crease in serum creatinine was associated with increased
inpatient mortality.12
Prophylaxis
AKI, of any cause, increases the risk of developing CKD. CKD
increases the need for RRT and has increased mortality. There
are no suitably powered studies to date that demonstrate that
prevention of CA-AKI improves mortality, but it does reduce
the incidence of AKI and CKD. Although not proved specif-
ically in CA-AKI, reducing the incidence of AKI may improve
longer term outcomes by reducing CKD and mortality.
A pragmatic approach to patients undergoing contrast-
enhanced procedures should include the use of evidence-
based preventative measures in those at highest risk for AKI.
Burdensome interventions should be avoided if unnecessary.
A large number of interventions have been evaluated in the
Table 2 Risk factors for CA-AKI with percutaneous coronary
interventions (reproduced and adapted with permission)9
Risk factor Relative
integer score
Hypotension (systolic BP<80 mmHg 5
requiring inotropic drugs)
Intra-aortic balloon pump 5
Congestive cardiac failure (NYHA 5
classification III/IV, history of pulmonary
oedema, or both)
Age >75 yr 4
Anaemia (baseline haematocrit<39% male, 3
<36% female)
Diabetes 3
Contrast media volume 1 for each 100
ml
Creatinine 133 mmol L1 4
or
eGFR
40e60 ml min1 1.732 2
20e40 ml min1 1.732 4
<20 ml min1 1.732 6
BJA Education - Volume 20, Number 12, 2020 419
Acute kidney injury
Table 3 CA-AKI risk scoring model for percutaneous coronary
interventions (reproduced and adapted with permission)9
Risk score Risk of CA-AKI (%) Risk of needing RRT (%)
5 7.5 0.04
6e10 14.0 0.12
11e16 26.1 1.09
16 57.3 12.6
prevention of CA-AKI. Intravascular volume expansion is the
only intervention with definitive benefit.
Numerous bodies have published guidelines in an effort to
reduce the incidence of CA-AKI, including the American Col-
lege of Radiology (ACR), the European Society of Urogenital
Radiology, KDIGO, the National Institute for Health and Care
Excellence (NICE) and the Renal Association. Many of these
guidelines are based on expert opinion with poor quality data,
using studies without control groups.
Contrast agent
Modifiable factors are to minimise the volume of contrast
agent, using low osmolarity or iso-osmolar contrast, and using
non-iodinated contrast media. The volume of contrast agent
given correlates with the risk of CA-AKI.13
Fluids
Intravascular volume expansion at the time of giving contrast
may counteract both the indirect intra-renal haemodynamic
changes and direct renal tubular toxic effects of contrast. It
may reduce cellular damage by diluting the tubular concen-
tration of contrast agent and is likely to decrease tubular fluid
viscosity. Possibly more importantly, it may correct and
optimise other concurrent causes of AKI, unrelated to giving
contrast, such as dehydration.
Intravascular volume should be optimised in any patient
receiving contrast. The exact volume and rate of fluids given is
probably less important, but should be individualised to ach-
ieve euvolaemia. Oral fluid is adequate for those at low risk of
CA-AKI and i.v. fluids are preferred for high-risk patients.
Regarding i.v. fluids, isotonic sodium bicarbonate or isotonic
sodium chloride could be used; the former may have addi-
tional benefits (discussed later), but the ideal rate and volume
remains unclear. Exact fluid type should be considered in the
context of any electrolyte and acid-base derangements. Evi-
dence suggests that giving fluids reduces the incidence of CA-
AKI but has minimal effect on the use of RRT or mortality.4
Oral hydration is not considered inferior to i.v. hydration at
preventing CA-AKI.1 NICE recommends encouraging oral hy-
dration before and after contrast agent exposure in adults at
risk of CA-AKI in both outpatients and inpatients if appro-
priate. Outpatient hydration needs to be pragmatic and avoid
unnecessary prolonged admission for i.v. fluids. It would seem
reasonable to encourage oral fluid intake in the preoperative
setting, whilst adhering to existing ‘nil-by-mouth’ guidelines.
One study provided 500 ml water in the 4 h before giving
420 BJA Education - Volume 20, Number 12, 2020
contrast, stopping 2 h before the procedure and then another
600 ml water after contrast.14
NICE and KDIGO recommend i.v. rather than oral hydra-
tion for those at high risk of CA-AKI. Many varying regimes
have been trialled with i.v. fluids, commonly including an
infusion commencing 1 h before contrast agent administra-
tion and continuing for 3e6 h thereafter.4 Longer regimens (12
h post-contrast administration) have been shown to lower the
incidence of AKI further.15 Achieving a urine output >150 ml
h1 for 6 h after giving contrast was associated with a reduced
incidence of AKI.16 In some emergency circumstances it may
not be feasible to optimise fluid status before giving contrast,
but correction of hypotension should be attempted and fluids
should be given afterwards. Forced euvolaemic diuresis with
furosemide or mannitol has been shown to increase the
incidence of CA-AKI.17
It is unclear what volume of i.v. fluid is best to prevent AKI.
ACR guidelines recommend the use of i.v. saline 0.9% at 100 ml
h1 for 6e12 h before and 4e12 h after angiography.18 Euro-
pean Society of Cardiology guidelines advocate i.v. saline 0.9%
at 1e1.5 ml kg1 h1 for 12 h before and up to 24 h after the
procedure.7 The Prevention of Contrast Renal Injury with
Different Hydration Strategies (POSEIDON) trial showed fluid
titration to targeted left ventricular end diastolic pressures
had a lower incidence of CA-AKI compared with the control
group.19 Fluid should be administered judiciously in those at
risk of fluid overload, for example concurrent heart failure or
the elderly, who may develop pulmonary oedema, although
the POSEIDON trial demonstrated a low incidence of adverse
effects. However, the A Maastricht Contrast-Induced Ne-
phropathy Guideline (AMACING) trial randomly assigned 660
patients deemed high risk for CA-AKI undergoing contrast
procedures to receive either periprocedural i.v. isotonic saline
or no i.v. fluids.20 There was no significant difference in the
incidence of AKI between the hydration group and the no
hydration group. It should be noted that the AMACING trial
excluded those with eGFR<30 ml min1 1.732, thereby omit-
ting those potentially at highest risk of developing CA-AKI.
Most guidelines recommend i.v. hydration with either
isotonic (1.26%) sodium bicarbonate or isotonic (0.9%) sodium
chloride. The Prevention of Serious Adverse Events Following
Angiography (PRESERVE) study showed equivalent values of
i.v. isotonic sodium bicarbonate and isotonic sodium chloride
in patients at high risk of CA-AKI after angiography (CA-AKI in
9.5% vs 8.3%, respectively [p¼0.13]).21 Sodium bicarbonate may
have additional therapeutic benefits, including urinary alka-
lisation and free radical scavenging, but a meta-analysis of
5686 patients showed no clinical benefit of sodium bicarbon-
ate over sodium chloride.22 We are not aware of any trial that
has compared giving a balanced crystalloid fluid with isotonic
saline or isotonic sodium bicarbonate, despite the proved
benefits of these fluids in other settings.
Pharmaceutical agents
N-acetylcysteine (NAC) has been extensively investigated for
the prevention of CA-AKI. Data fails to provide a significant
benefit in clinical outcomes, with either oral or i.v. NAC
administration.21 NAC is not widely used in the UK and not
recommended by NICE, but it is by KDIGO, despite having no
effect on mortality, AKI or need for RRT.
 Acute kidney injury

Contrast-enhanced scan or procedure required.

Consider alternative imaging techniques

Time-critical emergency scan or

Emergent or elective scan
intervention

Proceed to scan, do not await renal Consider and discuss in MDT:

function tests if time-critical • Probability and importance of accurate
Optimise intravascular volume status diagnosis and risk of misdiagnosis
before and after contrast (with i.v. • Alternative methods of diagnosis
isotonic saline or sodium bicarbonate), • Baseline renal function (eGFR)
avoid nephrotoxic agents, minimise • Allergic reaction risk
contrast dose

If appropriate, proceed to scan/intervention,

Closely follow up consider baseline risk factors, use risk
renal function tests (Day 3 minimum) prediction tools (e.g. Mehran).

High risk of CA-AKI Low risk of CA-AKI

(including eGFR<59 ml min–1 1.73–2, (including eGFR>60 ml
recent AKI): min–1 1.73–2):
Discuss in MDT, optimise Consider elements of
intravascular volume status before ‘high risk’ to adopt if
and after contrast (with i.v. isotonic appropriate, oral hydration
saline or sodium bicarbonate), pre- and post-contrast
avoid nephrotoxic agents,
minimise contrast dose

Follow up renal
function tests (Day 3 minimum)

Fig 1 Decision-making aid for patients needing contrast-enhanced imaging or intervention.

There is insufficient evidence to support stopping di-
uretics, angiotensin-converting enzyme inhibitors or angio-
tensin receptor blockers. NICE advises consideration of
temporarily stopping these medications in those with CKD
with eGFR<40 ml min1 1.732.1 It seems appropriate to avoid
and stop nephrotoxic medications around the time of giving
contrast agent, including NSAIDs. Metformin is not itself
nephrotoxic but there is risk of developing lactic acidosis in
severe AKI and it is advised to temporarily stop metformin
after contrast is given.
Renal replacement therapy
Use of prophylactic RRT is not recommended for removing
contrast agent, even in those at high risk of CA-AKI. Contrast
agents are excreted predominantly by glomerular filtration,
and elimination is delayed in those with renal dysfunction.23
Some 60e90% of contrast agent can be effectively removed
by intermittent haemodialysis. However, evidence does not
demonstrate a reduction in the incidence of CA-AKI with
prophylactic RRT use after giving contrast agents and it is
currently not recommended by KDIGO.
Influence on decision making
Regardless of whether AKI after contrast is a marker or a
mediator of adverse outcomes, it has an impact on clinical
practice. Unnecessarily avoiding or postponing a contrast
scan or procedure may deny or delay an accurate diagnosis or
treatment. Patients with CKD are less likely to undergo coro-
nary angiography than those with normal renal function and
this may be partly because of concerns over CA-AKI.24
Avoiding contrast in patients with CKD occurs with other
contrast-enhanced procedures. The topic is complex as this
may equally signify the appropriate use of alternative imaging
modalities that avoid contrast.

BJA Education - Volume 20, Number 12, 2020 421

Acute kidney injury
The use of a contrast agent in patients with CKD or high
risk of CA-AKI should be discussed as part of an individualised
multidisciplinary team discussion, including the patient, a
renal physician, the radiologist and referring clinician. NICE
recommends discussion with renal physicians in those on
RRT (those with residual urine output may require dialysis
after contrast) or with a renal transplant, but again this should
not necessarily delay emergency imaging.1 A threshold
eGFR<30 ml min1 1.732 or a recent AKI are recommended by
ACR as a trigger for discussion between the radiologist and
referring clinician.18
We propose a logical approach to management of patients
receiving a contrast agent (see Fig. 1).
Special circumstances
Gastrointestinal surgery
A recent prospective cohort study of more than 5000 patients
undergoing both elective and emergency abdominal surgery
found an overall incidence of AKI of 13.4%.25 There was no
increased risk of postoperative AKI in those exposed to pre-
operative i.v. contrast scans (n¼1249) using a propensity
score-matched model.
Endovascular aneurysm repair
AKI after endovascular aneurysm repair and open aortic
aneurysm repair is common and multifactorial; the incidence
varies (up to 36%) because of differing definitions of AKI in the
literature, but is most common in emergency open repair.26
There are multiple risk factors for AKI after endovascular
aneurysm repair including: emergency procedures; guidewire
manipulation in the renal vessels; embolisation of athero-
matous plaque into renal vessels; perioperative hypotension;
and the use of contrast. Significant AKI after AAA repair is
associated with increased mortality. The same principles
apply to reducing the risk of AKI as discussed previously.
Paediatrics
Risk factors for AKI in children include prematurity, postnatal
infections, congenital heart disease and congenital kidney
diseases. Children with these conditions are more likely to
require contrast-enhanced scans and interventions. There are
few studies examining CA-AKI in paediatric patients. Paul and
colleagues found no AKI development in severely injured
children after i.v. contrast for CT scanning.27 Preventative
measures are largely extrapolated from adult research and
clinical practice but lack primary evidence in the paediatric
population.
Intensive care
Critically ill patients are at high risk of developing AKI for
multiple reasons. A propensity score matched non-
randomised trial of patients in ICU found an increased risk
of AKI and dialysis in the contrast vs non-contrast group if
eGFR was <45 ml min1 1.732.28 However, without properly
controlled studies, it is difficult to ascertain the significance of
contrast agents in causing AKI in heterogeneous patients in
ICU.
422 BJA Education - Volume 20, Number 12, 2020
Gadolinium-based contrast agents (GBCAs)
Gadolinium chelates are used as a contrast agent in MRI scans.
GBCAs in high doses are nephrotoxic, causing CA-AKI.29 The
incidence of CA-AKI and allergic reaction are much lower with
GBCAs than iodinated contrast agents. The Royal College of
Radiologists recommends caution when using GBCAs in those
with renal dysfunction and alternative imaging techniques
should be considered. If needed, minimising the dose of GBCA
will reduce the risk of CA-AKI.
Nephrogenic systemic fibrosis (NSF) is a rare, but serious
disorder that occurs in those with impaired renal function
when exposed to GBCAs. Collagen disposition results in con-
tractures and fibrosis of multiple systems: lung, liver, heart
and muscle. Current GBCAs pose a much lower risk than
historic agents; there is a <1% risk of developing NSF with
newer GBCAs in those with renal dysfunction.30 To reduce the
risk of NSF the GBCA dose should be limited, lower-risk GBCAs
used, repeat contrast administration avoided within 7 days
and GBCAs avoided in patiens with AKI. Initiation of inter-
mittent haemodialysis is not recommended, but for those
already on it, they should be dialysed within 24 h of giving a
GBCA.
Conclusions
CA-AKI remains one of the leading causes of AKI, but its val-
idity remains a clinical and research dilemma. To date, no
RCTs have been performed to truly elucidate whether CI-AKI
exists. The historically high incidence of CA-AKI is now
much lower than previously reported. Iso-osmolar and low
osmolality contrast agents do not appear to be significantly
nephrotoxic. AKI does occur after the use of contrast, but this
is likely to reflect multifactorial mechanisms, particularly in
patients who are critically ill or those with significant risk
factors.
We recommend proceeding with a contrast scan or inter-
vention in the emergency setting, if deemed appropriate, and
alternative imaging is not suitable, especially if i.v. contrast is
given. An evidence-based multidisciplinary team discussion
in elective situations is essential to highlight those at high risk
of CA-AKI and weigh up the risks and benefits of obtaining an
accurate diagnosis. In both settings, it is important to limit the
dose and volume of contrast agent, and CA-AKI prophylaxis,
namely intravascular volume expansion, should be given to
those at high risk, with close follow-up of renal function.
MCQs
The associated MCQs (to support CME/CPD activity) are
accessible at www.bjaed.org/cme/home by subscribers to BJA
Education.
Acknowledgements
The authors would like to thank Professor Coralie Bingham
FRCP PhD (honorary associate professor and consultant in
renal medicine, Royal Devon & Exeter NHS Foundation Trust,
UK) for reviewing this article before submission.
Declaration of interests
The authors declare that they have no conflicts of interest.

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