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Journal of Clinical Nephrology and Research
Review Article
How to Prevent ContrastInduced Nephropathy in Clinical
Practice
Michele Andreucci1*, Teresa Faga1, Massimo Sabbatini2, Antonio
Pisani2, Domenico Russo2 and Ashour Michael1
1
2
Abstract
After the description of the Contrast-Induced Nephropathy (CIN), its epidemiology
and its pathogenesis, the risk factors for the development of CIN are discussed in
depth, the main ones being pre-existing renal impairment, particularly secondary to
diabetic nephropathy, salt depletion and dehydration, congestive heart failure, age
greater than 70 years and concurrent use of nephrotoxic drugs. Then the measures
to prevent CIN are suggested, beginning with the main rules in prevention: monitoring
renal function, discontinuation of potentially nephrotoxic drugs, use of either iodixanol,
an iso-osmolar contrast medium or iopamidol, a low-osmolar contrast medium at the
lowest dosage possible. The main procedure for prevention of CIN is an adequate
hydration of the patient with either isotonic sodium chloride or sodium bicarbonate
solutions. The antioxidant N-acetylcysteine may be added orally or intravenously.
Other antioxidants, such as vitamin C (ascorbic acid) and vitamin E (a- or γ-tocopherol),
compounds with antioxidant properties (e.g. Mesna), and β1-adrenergic receptor
antagonists (e.g. Nebivolol) require further studies before deciding their use in clinical
practice to prevent CIN.
CIN: Contrast-Induced Nephropathy; CI-AKI: ContrastInduced Acute Kidney Injury; CT: Computed Tomography; MDRD:
Modification of Diet in Renal Disease; eGFR: Estimated Glomerular
Filtration Rate; LOCM: Low-Osmolar Contrast Media; NO: Nitric
Oxide; ROS: Reactive Oxygen Species; SOD: Superoxide Dismutase;
MBL: Mannose-Binding Lectin; HOCM: High-Osmolar Contrast
Media; IOCM: Iso-Osmolar Contrast Media; Mesna: MercaptoEthane-Sulfonate Na; MASP-2: Mbl-Associated Serine Proteases-2;
MRI: Magnetic Resonance Imaging
CONTRAST-INDUCED NEPHROPATHY (CIN)
Contrast-Induced Nephropathy (CIN; other definition: ContrastInduced Acute Kidney Injury - CI-AKI) is an iatrogenic disease
that may occur when radiographic contrast media are injected
intravenously or intra-arterially to improve the visibility of internal
organs and structures in X-ray based imaging techniques, such as
radiography and Computed Tomography (CT), or for percutaneous
coronary intervention using contrast agents. It may be so defined
in any case of acute renal failure occurring (especially in patients
with pre-existing renal impairment and in those with diabetes) [1]
within 48-72 hrs of exposure to intravascular radiographic contrast
agents that cannot be attributed to other causes. It is usually a
nonoliguric acute renal failure with asymptomatic transient decline
Submitted: 18 March 2014
Accepted: 27 June 2014
Published: 30 June 2014
Copyright
© 2014 Andreucci et al.
OPEN ACCESS
Keywords
Department of Health Sciences, Magna Graecia University, Italy
Department of Public Health, Federico II University, Italy
ABBREVIATIONS
*Corresponding author
Michele Andreucci, Department of Health Sciences,
Magna Graecia University, Nephrology Unit, Campus
Salvatore Venuta, Viale Europa, loc. Germaneto,
I-88100 Catanzaro, Italy, Email:
•Contrast-Induced Nephropathy
•Contrast-Induced Acute Kidney Injury
•Acute Renal Failure
•Radiographic contrast media
•Iodinated contrast material
•Renal cells
•Renal injury
in renal function, occurring generally within 48-72 hrs of contrast
administration, peaking on the third to fifth day, and returning to
baseline within 10–14 days [2]. It is mirrored by an absolute (0.5
mg/dl or greater) or relative (by 25% or greater) increase in serum
creatinine from baseline [3,4] or, better, by a decrease (to 30-60
mL/min - renal insufficiency – or less) in the estimated glomerular
filtration rate (eGFR), i.e. the creatinine clearance calculated using
the MDRD (Modification of Diet in Renal Disease) calculation [5]
or the very simple Cockcroft-Gault formula [6]. The risk for CIN in
outpatients with an eGFR greater than 45 ml/min per 1.73 m2 seems
to be extremely low, estimated to be in the region of about 2% [7].
In 10% of patients with pre-existing renal failure undergoing
coronary angiography [8] and in <1% of all patients undergoing
percutaneous coronary intervention using contrast agents [9] CIN
may cause a severe acute renal failure with oliguria (<400 mL/24 hrs)
requiring dialysis, which is accompanied by a high mortality rate. The
management of CIN is the same as that for acute renal failure due to
other causes [10-12].
In order to determine the effect of Intravenous (IV) Low-Osmolar
Contrast Media (LOCM) on the development of post-CT CIN,
Davenport et al [13] performed a retrospective study. In 20,242 adult
in patients undergoing CT examinations over a period of 10 years
(10,121 untreated and 10,121 treated with IV contrast media, stratified
Cite this article: Andreucci M, Faga T, Sabbatini M, Pisani A, Russo D, et al. (2014) How to Prevent Contrast-Induced Nephropathy in Clinical Practice. J Clin
Nephrol Res 1(1): 1002.
Andreucci et al. (2014)
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by pre-CT stable eGFR) observed that IV LOCM is a risk factor for
nephrotoxicity in patients with a stable eGFR <30 mL/min/1.73 m2;
there is a trend toward significance at 30-44 mL/min/1.73 m2; it does
not appear to be a nephrotoxic risk factor in patients with a pre-CT
eGFR >45 mL/min/1.73 m2 [13,14].
In another recent retrospective study involving 53,439 patients in
whom serum creatinine (ranging between <1,5 and >2 mg/dL) was
regularly checked to determine the effect of IV iodinated contrast
material exposure to the incidence of CIN, McDonald et al [15] found
that the incidence of CIN was not significantly different between the
contrast group and control group. Thus, they suggest that intravenous
iodinated contrast agents are not the cause of decreased renal function
after contrast material administration.
In a systematic review and meta-analysis of controlled studies
the same authors [16] examined the incidence of CIN in patients
exposed to IV contrast medium compared with patients without
contrast (control group); they demonstrated a similar incidence of
CIN, dialysis, and death between the contrast group and control
group [16].
Among all procedures utilizing contrast agents for either
diagnostic or therapeutic purposes, coronary angiography and
percutaneous coronary interventions are associated with the highest
rates of CIN [4]. This is mainly related to (a) the intra-arterial
injection, (b) the high dosage of the contrast used and (c) the type of
patients who are usually in advanced age, with one or more comorbid
conditions, such as advanced vascular disease, severe long-standing
hypertension and diabetes [7].
The relationship of CIN to long-term adverse events (e.g. death,
stroke, myocardial infarction, end-stage kidney disease, percutaneous
coronary revascularization, coronary artery bypass graft surgery,
cardiac arrest, etc) has been studied in 294 patients, with follow-up of
at least 1 year after contrast exposure. The rate of long-term adverse
events was higher in individuals with CIN [17].
Pathogenesis
The mechanisms of nephrotoxicity by contrast agents are not
fully understood [18]. It can be reasonably assumed that CIN is due
to many factors, including an initial increase followed by a more
prolonged decrease in renal blood flow, a decrease in glomerular
filtration rate, a decrease in Nitric Oxide (NO) and a severe reduction
in medullary blood flow with renal ischaemia, hypoxia and direct
tubular damage, formation of Reactive Oxygen Species (ROS) [1923], increased intratubular pressure secondary to contrast-induced
diuresis, increased urinary viscosity and tubular obstruction,
all frequently associated with dehydration and a decrease in the
effective intravascular volume [2,10,24]. In vivo experiments in
rats have demonstrated that the decrease in cortical and medullary
microvascular blood flow induced by contrast media is partly
accounted for by the downregulation of endogenous renal cortical
and medullary NO synthesis [25]. To support the role of ROS
generated in contrast media-induced vasoconstriction, the use of the
Superoxide Dismutase (SOD) mimetic Tempol reduced iodixanolinduced vasoconstriction [26]. More recent work using a recombinant
manganese SOD administered in vivo to rats undergoing diatrizoate
treatment caused an improvement in GFR and a reduction in renal
histologic damage [27].
J Clin Nephrol Res 1(1): 1002 (2014)
Direct toxicity on tubular epithelial cells by contrast agents has
been observed in studies of isolated tubule segments and cultured cells
causing disruption of cell integrity, generation of ROS and apoptosis.
Contrast agents cause cellular damage to endothelial cells, i.e. the first
cells to come in contact with intravenously-injected contrast agents
[2]. The contrast agents are then filtered by glomeruli and become
concentrated within the tubules, thereby exposing the tubular cells
to an even worse direct damage [28]. In vitro cell culture studies have
shown that all types of contrast agents cause a decrease in cell viability
[29-33]. The biochemical changes underlying these effects have
been extended to studying changes in major intracellular signalling
pathways involved in cell survival, death and inflammation [31-36]
in vitro in cultured renal tubular cells [37-39]. Contrast media can
cause perturbation of mitochondrial enzyme activity and apoptosis
[40]. Studies in animals as well as in vitro studies suggest, in fact, that
they can directly induce caspase-mediated apoptosis of renal tubular
cells [41-46].
Some studies have demonstrated the crucial role played by
mannose-binding lectin (MBL, a protein of the lectin pathway of
the complement system) in aggravating the inflammatory response
and the tissue damage during ischemia/reperfusion injury of several
organs, including the kidney [47,48], that is alleviated by inhibition
with C1 inhibitor, a potent MBL and lectin pathway inhibitor [49].
In experimental ischemia/reperfusion models, MBL has been found
to induce tubular cell death, independent of the complement system,
and contribute to endothelial dysfunction, after binding to vascular
endothelial cells, by triggering a pro-inflammatory reaction [50-52].
Urinary MBL is increased after administration of contrast agents and
in humans with CIN, suggesting some role of MBL in causing CIN
[49,53]. In a trial assessing the importance of serum MBL for the
development of CIN, the deficiency of this lectin did not influence the
occurrence of CIN as defined by a serum creatinine increment; but it
was associated with an increase in cystatin C after the administration
of a contrast agent [54]. We have to consider that the increase of
serum creatinine after contrast media is delayed, usually achieving
a maximum two to five days after contrast exposure. Serum cystatin
C, instead, is a more sensitive marker and has been shown to increase
earlier, to peak 24 hours after contrast administration, thereby
detecting even subtle changes in eGFR after acute kidney injury
including CIN [55-58]. Thus, in this clinical trial, subjects with MBL
deficiency were almost two-times less likely to develop an increase
of ≥10% in cystatin C after administration of the contrast agent.
This suggests that deficiency of MBL might attenuate some of the
detrimental effects of contrast media [54].
Identification of patients at high risk for the
development of CIN
The European Society of Urogenital Radiology has suggested
that the real risks for CIN are represented by pre-existing renal
impairment, particularly secondary to diabetic nephropathy, salt
depletion and dehydration, congestive heart failure, an age greater
than 70 years and concurrent use of nephrotoxic drugs [3,59].
Undoubtedly, pre-existing impairment of renal function,
irrespective of cause, represents the main risk factor for CIN. The
lower the eGFR, the greater is the risk of CIN. An eGFR of 60 ml/
min/1.73m2 is a reliable cutoff point for identifying patients at high
risk for the development of CIN [2]. The incidence of CIN in patients
with chronic renal failure ranges from 14.8 to 55% [4]. Diabetes
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mellitus is the second most important factor predisposing to CIN,
particularly when associated with renal insufficiency [60]. At any
given degree of baseline eGFR, diabetes doubles the risk of developing
CIN. The incidence of CIN in diabetic patients varies from 5.7 to
29.4% [4,61,62]. he coupling of chronic kidney disease and diabetes,
however, dramatically increases the risk for CIN compared with
that observed for chronic kidney disease alone [63]. Another risk
factor for CIN is the concomitant use of nephrotoxic drugs, such
as aminoglycosides, cyclosporin A, amphotericin, cisplatin and
nonsteroidal anti-inflammatory drugs [64,65] that should possibly
be discontinued before radiocontrast administration [2]. The role of
renin-angiotensin-aldosterone system blocking agents (angiotensinconverting enzyme inhibitors and angiotensin II receptor blockers) in
the pathophysiology of CIN is still controversial [66]. Many authors
believe that these drugs should be discontinued in patients with
chronic renal disease at high risk for developing CIN [67-73]. Others
deny a negative influence in the incidence of CIN in stable patients
with chronic renal failure [74]. KDIGO does not deem it necessary
to discontinue these medications prior to contrast administration
[75]. Other risk factors include: prolonged hypotension [10,76],
severe dehydration, reduction of effective intravascular volume due
to congestive heart failure, liver cirrhosis, or salt depletion secondary
to abnormal fluid losses associated with insufficient salt intake
[10,22,79-78].
CIN was first described in a patient with multiple myeloma
receiving intravenous pyelography [79]. Today the incidence of CIN
in patients with multiple myeloma with a normal serum creatinine
is believed to be low and correlated with β2-microglobulin levels,
making the administration of contrast agents relatively safe [80].
Table 1: Iodinated Contrast Media Commonly Used in Clinical Practice.
Name
mOsm/kg
Osmolality type
Metrizoate Isopaque (Conray 370)
2,100
HOCM
Ioxaglate (Hexabrix)
580
LOCM
Diatrizoate (Hypaque 50)
1,550
HOCM
Iopamidol (Isovue-370)
796
LOCM
Iodixanol (Visipaque 320)
290
IOCM
Iohexol (Omnipaque 350)
884
LOCM
Osmolality of contrast media compared with the osmolality of plasma.
HOCM: High-Osmolar Contrast Media, the highest osmolality, 5–8 times
the osmolality of plasma.
LOCM: Low-Osmolar Contrast Media, an osmolality 2–3 times the
osmolality of plasma.
IOCM: Iso-Osmolar Contrast Media, the same osmolality as plasma.
a dehydrating effect, particularly when high doses are given as during
cardiac catheterization procedures. Thus, the high incidence of CIN
might be the result of this side effect explaining the beneficial effects
of prophylactic hydration in preventing CIN [97].
It has been shown that the use of LOCM rather than HOCM is
beneficial in preventing CIN in patients with pre-existing renal failure
[98-101]. However, other studies comparing HOCM and LOCM
have shown a much less than anticipated advantage for the ability of
LOCM to decrease the risk of CIN, even in subjects with pre-existing
renal impairment [93,97,100]. Recent studies and meta-analyses have
found no significant difference in the rates of CIN between IOCM
and LOCM [102-105]; only that the LOCM iohexol seems to be more
nephrotoxic [98,106].
Other important risk factors include: advanced age [4,81], anemia
[82], severe congestive heart failure or compromised left ventricle
systolic performance [4], sepsis [10,65,81] and renal transplant [83].
MEASURES TO PREVENT CIN
Radiographic procedures, chemical characteristics
and route of administration of contrast media as risk
factors for the development of CIN
The first general rule of prevention is that in any patient
undergoing any radiographic procedure, renal function should be
monitored by measuring serum creatinine and calculating the eGFR.
This is even more important in patients at high risk of CIN, in whom
serum creatinine and eGFR should be checked before and once daily
for 5 days after the radiographic procedure [10].
Use of large doses of contrast media (e.g. in coronary angiography)
and their multiple injections within 72 hrs [10,81,84] represent risks
for CIN that is dose-dependent [9,85-88]. Radiographic contrast
media seem to be more nephrotoxic when given intra-arterially
because of the higher acute intrarenal concentration [10,89],
particularly if the arterial injection is suprarenal [1, 90-96].
The contrast agents have different osmolalities (number of
molecules per kilogram of water), greater than that of plasma (Table
1). Ionic High-Osmolar Contrast Media (HOCM, e.g. diatrizoate)
have an osmolality of 1500 to 1800 mOsm/kg (i.e. 5–8 times the
osmolality of plasma); nonionic Low-Osmolar Contrast Media
(LOCM e.g. iohexol) have an osmolality of 600 to 850 mOsm/kg (i.e.
2–3 times the osmolality of plasma); nonionic Iso-Osmolar Contrast
Media (IOCM e.g. iodixanol) have an osmolality of approximately
290 mOsm/kg (i.e. same osmolality as plasma). Ionicity is the
characteristic of a molecule to break up into a cation and an anion,
resulting in more molecules per kilogram of water, thereby increasing
osmolality. Nonionic agents not having this property are less osmolar
[2].
All iodinated radiocontrast media are osmotic diuretics. The
higher osmolality the greater is the diuresis. This osmotic diuresis has
J Clin Nephrol Res 1(1): 1002 (2014)
Main rules in prevention of CIN
The second rule is that potentially nephrotoxic drugs should
be discontinued before the contrast procedure. We refer to
aminoglycosides, vancomycin, amphotericin B, metformin and
nonsteroidal anti-inflammatory drugs [2]. Sometimes aminoglycosides
are necessary and cannot be discontinued. For these conditions the
European Renal Best Practice position [107] is “not using more than
one shot of aminoglycosides for the treatment of infections… in
patients with normal kidney function in steady state, aminoglycosides
are administered as a single-dose daily rather than multiple-dose…
monitoring aminoglycoside drug levels”. For amphotericin B, the
ERBP recommends that saline loading be implemented in all patients
receiving any formulation of amphotericin B [107]. The potential
harm by metformin (an oral antihyperglycemic medication, used to
treat type II diabetes, that stimulates intestinal production of lactic
acid) is the severe lactic acidosis that may follow the occurrence of
renal failure (since metformin is excreted unchanged almost entirely
by the kidneys, it is retained in case of CIN); this lactic acidosis can
be fatal. Thus, the drug has to be discontinued at least 12 hours before
the contrast and not be resumed for a minimum of 36 hours after
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the procedure, or longer if the serum creatinine has not returned to
baseline [108].
The third rule is the choice of the least nephrotoxic radiocontrast
agent. LOCM (e.g. iohexol) are less nephrotoxic than HOCM (e.g.
diatrizoate). Moreover, IOCM (e.g. iodixanol) seem to be less
nephrotoxic than LOCM [10]. In a multicenter, randomized, doubleblind comparison of iopamidol (LOCM) and iodixanol (IOCM),
performed in patients with chronic kidney disease, the rate of CIN
was not statistically different after the intraarterial administration of
iopamidol or iodixanol to high-risk patients, with or without diabetes
mellitus [103]. Thus, iodixanol (IOCM) and iopamidol (LOCM)
appear to be contrast agents of choice to reduce risk of CIN.
The fourth rule is to use the lowest dosage possible of contrast
media. High doses of contrast agents are required in percutaneous
coronary intervention. For this procedure, some formulas have been
suggested to calculate the dosage that is least dangerous for renal
function:
(A) Cigarroa’s formula: 5 mL of contrast per kg b.w./Serum
Creatinine (mg/dL) with maximum dose acceptable of 300 mL for
diagnostic coronary arteriography [109].
(B) Laskey’s formula: volume of contrast to calculated creatinine
clearance ratio with a cut-off point of the ratio at 3.7 for percutaneous
coronary intervention; a ratio >3.7 would be associated, following
contrast use, with a decrease in creatinine clearance [110]; recently
the cut-off point has been placed at 2.0: below a ratio of 2.0 CIN
would be a rare complication of percutaneous coronary intervention,
but it would increase dramatically at a ratio of 3.0 [111,112].
(C) ratio of grams of iodine to the calculated creatinine clearance;
a ratio of 1.42, or even better a ratio of 1.0, would prevent CIN [111].
Adequate hydration
The main procedure for prevention of CIN is an adequate
hydration of the patient [113,114]. The old suggestion to limit fluid
intake starting the day before contrast administration must be
abolished and replaced by volume supplementation: e.g. 500 mL of
water or soft drinks (e.g. tea) orally before and 2,500 mL for 24 hours
after contrast administration in order to secure urine output of at least
1 mL/min in a non-dehydrated patient [115]. In high-risk patients
adequate hydration may be obtained by IV infusion of 0.9% saline
at a rate of approximately 1 mL/kg b.w.per hour, beginning 6–12
hours before the procedure and continuing for up to 12–24 hours
after the radiographic examination; this may be done only if urine
output is appropriate and cardiovascular condition allows it [10,113].
The rationale for volume supplementation is that hydration causes
expansion of intravascular volume, suppression of renin-angiotensin
cascade and consequent reduction of renal vasoconstriction
and hypoperfusion. The resulting increase of diuresis will limit
the duration of contrast material contact with renal tubules and
consequently its toxicity on tubular epithelium [116,117].
Some clinical studies and meta-analysis have shown that sodium
bicarbonate hydration is superior to sodium chloride [118-126] at
least when using LOCM [127]. For patients undergoing an emergency
coronary angiography or intervention the following protocol has
been used: 154-mEq/L infusion of sodium bicarbonate as a bolus of
3 mL/kg b.w./hour for 1 hour before the administration of contrast,
followed by 1 mL/kg/hour for 6 hours during and after the procedure
J Clin Nephrol Res 1(1): 1002 (2014)
[119]. The rationale for using bicarbonate infusion is explained in
that any condition (such as acetazolamide administration or sodium
bicarbonate infusion) that increases bicarbonate excretion decreases
the acidification of urine and renal medulla. Consequently, this will
reduce the production and increase the neutralization of oxygen free
radicals, thereby protecting the kidney from injury by contrast agents
[121,122,1285,129].
Other investigators did not find a benefit with sodium
bicarbonate hydration versus sodium chloride [130-133]. Some
authors found even an increased incidence of CIN with the use of
intravenous sodium bicarbonate [134]. The ERBP “recommends
volume expansion with either isotonic sodium chloride or sodium
bicarbonate solutions, rather than no volume expansion, in patients
at increased risk for CIN” [107].
Antioxidants
Since ROS have been proved to play an important role in the renal
damage caused by iodinated radiocontrast agents, the antioxidant
N-acetylcysteine has been thought to act either as a free-radical
scavenger or as a reactive sulfhydryl compound as well as a factor
able to increase the vasodilating effect of NO [10,21,135]. Shortduration pretreatment with N-acetylcysteine has been demonstrated
to reduce contrast-induced cytotoxicity in human embryonic kidney
cells treated with the ionic HOCM ioxithalamate, non-ionic LOCM
iopromide and the IOCM iodixanol [136] and to ameliorate the
ischemic renal failure in animal models [137]. Despite controversial
results observed in high risk patients [134,138-147], it has been
suggested to use N-acetylcysteine in high-risk patients either with
an oral dose of 600 mg twice daily the day before and the day of
procedure [10] or, in patients unable to take the drug orally, with an
IV dose of 150 mg/kg over half an hour before the procedure or 50
mg/kg administered over 4 hours [139].
Other antioxidants have been suggested for use against CIN:
vitamin C (ascorbic acid), vitamin E (α- or γ-tocopherol) and Mesna.
Conflicting results have been obtained with the use of ascorbic
acid [136,148-150] at a dosage of 3 g orally 2 hours before the
procedure and 2 g during the night and in the morning after the
procedure [148,149]. N-acetylcysteine (1,200 mg orally twice a day
before and on the day of coronary catheterization) has been shown to
be more beneficial in preventing CIN than ascorbic acid, particularly
in diabetic patients with renal insufficiency undergoing coronary
angiography [151]. In a recent meta-analysis, with 1536 patients who
completed the trial, patients receiving ascorbic acid had a 33% less
risk of developing CIN [152].
The oral administration of either 350 mg/day of α-tocopherol or
300 mg/day of γ-tocopherol (5 days prior to the coronary procedure
and continued for a further 2 days post-procedure) in combination
with 0.9% saline (1 mL/kg/h for 12 hours before and 12 hours after)
has been demonstrated to be effective in protecting against CIN in
patients with chronic kidney disease undergoing coronary procedures
with Iopromide (LOCM): CIN developed in 14.9% of cases in the
placebo group, but only in 4.9% and 5.9% in the α- and γ-tocopherol
groups, respectively [153].
Mesna (mercapto-ethane-sulfonate Na) is an agent with
antioxidant properties that has been shown to reduce free radicals and
restore reduced glutathione levels after ischemic renal failure [154].
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In a randomized controlled trial using Mesna for the prevention
of CIN, the IV administration of 1600 mg Mesna versus placebo,
together with intravenous hydration with 0.9% saline, resulted in the
occurrence of CIN in 7 patients in the placebo group and none in the
Mesna group [155]. Further studies would be necessary to confirm
such a positive outcome.
Nebivolol
Nebivolol, a third-generation β1-adrenergic receptor antagonist
[156,157], has been hypothesized to protect the kidney against
CIN through its antioxidant and NO-mediated vasodilating action
[158]. In experimental rats it has been shown to decrease medullary
congestion, protein casts and tubular necrosis, systemic and renal
oxidative stress, microproteinuria secondary to contrast media, and
to increase the kidney nitrite level decreased by contrast media [158].
Nebivolol (5 mg/day for one week or 5 mg every 24 hours for 4 days)
decreased the incidence of CIN in patients with renal dysfunction
undergoing coronary angiography [159,160].
Statins
Recent studies have shown a beneficial effect of statins to
prevent CIN in patients undergoing percutaneous coronary
intervention [161-166]. This is not surprising, considering that
hypercholesterolemia has been suggested to be a predisposing factor
to CIN on the basis of a study in experimental CIN, characterized
by compromised NO synthesis and enhanced ROS generation [167].
But the nephroprotective effect of statins has been attributed to
their antioxidant, anti-inflammatory, and antithrombotic properties
and to their vasodilator property mediated by NO, that improves
renal microcirculation [168,169]. Rosuvastatin (10 mg/day for five
days, two days before, three days post the procedure) reduced the
risk of CIN in patients with diabetes mellitus and chronic kidney
disease undergoing coronary/peripheral arterial angiography [170].
Also simvastatin had a dose-dependent nephroprotective effect in
experimental rats treated with radiocontrast agents [168]. Patients
on pravastatin had an even lower incidence of CIN than patients
on simvastatin [171,172]. Short-term atorvastatin (40 mg/day 3
days before the procedure) and chronic atorvastatin therapy had a
protective effect on renal function after coronary angiography [173].
Patients undergoing percutaneous coronary intervention were given
short-term pretreatment with atorvastatin (80 mg 12 hours before
intervention with another 40-mg pre-procedure, followed by longterm treatment of 40 mg/day); this prevented CIN and shortened
hospital stay [174].
Steroids
It has been recently suggested that high-dose steroids (1 mg/
kg of oral prednisone, 12-24 hours before and 24 hours after the
angiographic procedure) given concurrently with IV saline (1 ml/kg/
hour of 0.9% saline, 12 hours before the procedure) may protect renal
tubules against either iodixanol or iohexol [175]. This is based on the
fact that steroids may have a favorable impact on inflammation and
on renal tubular cell apoptosis and necrosis, as observed in models of
renal ischemia-reperfusion in which dexamethasone had a protective
effect against injury [176].
Diuretics and Anp
Since enhanced transport activity with oxygen consumption is a
principal cause of renal hypoxia and both furosemide and mannitol
J Clin Nephrol Res 1(1): 1002 (2014)
reduce transport activity, it has been suggested to use furosemide or
mannitol (associated with saline infusion to prevent salt depletion)
to protect against CIN. Several studies, however, have demonstrated
either no effect in protecting against contrast media or even
deleterious effect of furosemide and mannitol on renal function [177179]. Thus, diuretics should be avoided before contrast exposure in
high-risk patients who are susceptible to volume depletion [67].
Use of Atrial Natriuretic Peptide (ANP) has also failed to protect
against CIN [179,180].
CALCIUM CHANNEL BLOCKERS
Calcium Channel Blockers have been hypothesized to have
protective effects against CIN. The rationale is the following:
Ca2+ overload is considered to be a key factor in CIN; the increase
in intracellular calcium provokes a vasoconstrictive response in
intrarenal circulation and would be an important mediator of
epithelial cell apoptosis and necrosis. The Na+/Ca2+ exchanger system
is one of the main pathways of intracellular Ca2+ overload. It has
been demonstrated that in rats the pretreatment with KB-R7943, an
inhibitor of the Na+/Ca2+ exchanger system, significantly and dosedependently suppresses the increase of serum creatinine following
diatrizoate administration [181]. Hence, the use of Calcium Channel
Blockers has been suggested for prevention of CIN, but their use
has given controversial results, sometimes protective [182,183] and
sometimes with no benefit at all [177,184-186].
Other substances
Urinary adenosine is increased after contrast medium
administration: thus, it has been thought that Adenosine Antagonists
(theophylline, aminophylline) could have protective effects against
contrast media; but their use has given controversial results. Some
authors have observed beneficial effects against CIN [187-190], others
have denied any beneficial results [191,192].
Dopamine and Dopamine Agonists (e.g. fenoldopam, a selective
dopamine-1 receptor agonist with vasodilatory properties) have
given controversial results in protecting against CIN, some positive
[193-195], others negative [142,179,192,193,196,197]. On the basis of
our present knowledge, it is better to avoid them, considering their
adverse effects (arrhythmia with dopamine, and systemic hypotension
with intravenous fenoldopam).
The plasma and urine levels of endothelin-1 are increased in
diabetes and after exposure to high doses of contrast media; this
has suggested a role of endothelin-1 in diabetic nephropathy and in
CIN [22,198,199]. However, endothelin Receptor Blockers have been
proven deleterious as a prophylactic tool against CIN [200].
Prostaglandin E1 has given some positive protective results on
renal function following contrast medium injection in patients with
preexisting renal impairment [201], whilst L-arginine has shown no
benefit or even harm [202].
There are some experimental substances that seem promising in
preventing CIN, but require further evaluation. Thus, sodium butyrate
has been shown to decrease the activation of Nuclear Factor kappa B
(NF-κB), thereby reducing inflammation and oxidative damage in the
kidney of rats subjected to CIN [203]. Similarly, the human serum
albumin–Thioredoxin (HSA–Trx) has been demonstrated to prevent
CIN and renal tubular apoptosis, via its extended antioxidative action,
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in a rat model of ioversol-induced CIN [204]. Thioredoxin-1 – Trx - is
a ubiquitous low-molecular-weight protein, produced in the human
body in response to oxidative stress conditions. Finally, as already
mentioned, an important role in CIN may be played by mannosebinding lectin (MBL), with observations that MBL and MASP-2
(MBL-associated serine proteases-2) were significantly upregulated in
the urine samples taken 12-18 hours after administration of contrast
media compared to the pre-procedural urine sample [53]. Treatment
with anti-MBL monoclonal antibodies or inhibitors of MASP might
be protective against contrast media in order to prevent CIN [49].
Haemodialysis or haemofiltration
It has been suggested to remove radiocontrast media by
haemodialysis or haemofiltration immediately after the radiographic
procedure. However, the extracorporeal removal of contrast agents
did not decrease the incidence of acute renal failure in highrisk patients [205-208]. The ERBP does “not recommend using
prophylactic intermittent haemodialysis or haemofiltration for the
purpose of prevention of CIN” [107].
Alternative imaging method
KDIGO guidelines for Acute Kidney Injury Work Group
has stated that we should “consider alternative imaging methods
in patients at increased risk for CI-AKI” [75]. In fact, Magnetic
Resonance Imaging (MRI) with Gadolinium-Based Contrast Agents
may be an alternative imaging method. Gadolinium-Based Contrast
Agents are not iodinated compounds; thus, there is no risk for CIN
[209]. However, the use of Gadolinium-Based Contrast Agents
may be associated with acute renal failure or nephrogenic systemic
fibrosis, i.e. a rare pathology that causes fibrosis of the skin and
connective tissues throughout the body involving several organs,
kidney included; this occurs particularly in patients with pre-existing
renal failure [210,211].
ACKNOWLEDGEMENT
Dr. Ashour Michael is recipient of an “Assegno di Ricerca”
(“Research Check”) for 2014 given by the “Magna Graecia” University
of Catanzaro (Italy).
M.A. has been recipient of a grant from the Italian Society of
Nephrology (“S.I.N.”) for the year 2012 and for a financial research
support from Amgen.
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Cite this article
Andreucci M, Faga T, Sabbatini M, Pisani A, Russo D, et al. (2014) How to Prevent Contrast-Induced Nephropathy in Clinical Practice. J Clin Nephrol Res 1(1):
1002.
J Clin Nephrol Res 1(1): 1002 (2014)
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