Download contrast media

NEFROPATIA
DA MEZZO DI CONTRASTO
Contrast-Induced Nephropathy
(CIN)
Dino Docci
U.O. Nefrologia e Dialisi
Ospedale M. Bufalini
CESENA
Section 4: Contrast-induced Acute Kidney Injury
(CI-AKI)
Kidney International Supplements (2012) 2, 69-88
BACKGROUND
… the Work Group believes that there is a need for a unifying definiton for all forms
of AKI and therefore proposes that the term contrast-induced acute kidney
injury (CI-AKI) be used for patients developing AKI secondary to intravascular
radiocontrast media exposure
Evolution of Contrast Media
1950s
I
1980s
I
I
1990s
I
I
I I
I
COO-Na+
I
I
I
I
Ionic Monomer
Nonionic Monomer
Nonionic Dimer
Diatrizoate
Iothalamate
Iopamidol, Iohexol,
Ioversol, Iopromide
Iodixanol
(Iotrolan)
I
I I
I
COO-Na+
I
I
Ionic Dimer
Ioxaglate
HOCM
LOCM
IOCM
(High-Osmolar CM)
(Low-Osmolar CM)
(Iso-Osmolar CM)
~1500-1800 mOsm/kg
~600-800 mOsm/kg
~300 mOsm/kg
Types of Contrast Media
Viscosity vs. Osmolality of CM
Viscosity, cps at 37°C
12
iodixanol
10
iotrolan
ioxaglate
8
iohexol
ioversol
6
diatrizoate
iopamidol
iopramide
4
iothalamate
2
0
0
400
800
1200
1600
Osmolality, mOsm/kg H2O
2000
Pathophysiological Impact of
Contrast Media Properties
Type
Iodine
content
Osmolality
Viscosity
HOCM
+
++++
+
LOCM
+
+
++
IOCM
+
-
+++
CONTRAST MEDIA
DIRECT TOXICITY TO
PROXIMAL
TUBULAR CELL
Vasopressin
release
TUBULAR INJURY
Vacuolization
(‘osmotic nephrosis’)
Necrosis
Apoptosis
Tubular obstruction
…
HEMODYNAMIC EFFECTS
Osmolality related
Osmotic
diuresis
RHEOLOGIC EFFECTS
Endothelial dysfunction
Adenosine
release
Endothelin
release
Viscosity related
Blood
viscosity
NO and PGs
synthesis
Tubular luminal
dilatation and
tubular-interstitial
pressure
Distal sodium delivery
(tubulo-glomerular feedback)
O2 consumption
due to sodium
reabsorption
O2 free-radicals generation
and release
Tubular fluid
viscosity
VASOCONSTRICTION
Reactivity to
Angio II
Urine
flow rate
Reduced medullary blood flow
Altered renal microcirculation
MEDULLARY
HYPOXIA
Renal CM
retention
Decreased GFR
ACUTE RENAL FAILURE
Radiocontrast
Exposure
↑Adenosine
↑Endothelin
↑Vasopressin
↑Angiotensin?
↓Nitric Oxide
↓Prostaglandins
Intrarenal
vasoconstriction
Iodine toxicity, osmolality
Ionic strength
Altered
rheology
Osmotic
load
Endothelial
dysfunction
(DVR)
Reduced medullary
blood flow
↑O2
consumption
Medullary Hypoxia
Ischemic injury
to tuibular cells
CIN
Postischemic
oxydative
stress
Cytotoxicity
(proximal tubular cells)
Radiocontrast
Exposure
↑Adenosine
↑Endothelin
↑Vasopressin
↑Angiotensin?
↓Nitric Oxide
↓Prostaglandins
Intrarenal
vasoconstriction
Iodine toxicity, osmolality
Ionic strength
Altered
rheology
Osmotic
load
Endothelial
dysfunction
(DVR)
Reduced medullary
blood flow
↑O2
consumption
Medullary Hypoxia
Ischemic injury
to tuibular cells
CIN
Postischemic
oxydative
stress
Cytotoxicity
(proximal tubular cells)
CONTRAST-MEDIUM-INDUCED NEPHROPATHY:
CONSENSUS REPORT
Media Safety Committee of the ESUR)
A
(Contrast
DEFINITION
 A condition of acute deterioration of renal
function that occurs after iv administration of
contrast media in the absence of an alternative
etiology.
 Laboratory diagnosis is expressed as an
absolute increase (≥0.5 mg/dl) or a relative increase
(≥25%) in baseline serum creatinine concentration
48 to 72 hours after exposure to a contrast medium.
Morcos SK et al., Eur Radiol 9, 1602-1613 (1999)
Hospital Acquired Acute Renal Failure
(The Rush University Center experience)
Cause
Episodes
Decreased renal perfusion
Medications
Radiographic contrast media
Postoperative
Sepsis
Post-liver transplantation
Post-heart trasnplantation
Obstruction
Hepatorenal
147 (44%)
61 (18%)
43 (13%)
35
25
14
8
7
7
Nash K., Hafeez A., Hou S. Am J Kidney Dis 2002, 39: 930-936
Quantifying the problem
 Overall incidence is ~5%
 In patients with normal renal function, even in the
presence of diabetes, the incidence of CIN is negligible
(<1%)
 The incidence of CIN has been reported as high as 50%
for patients with multiple risk factors
Rudnick M.R., Goldfarb S., Tumlin J. Clin J Am Soc Nephrol 2008, 3: 261–262
Risk Factors for CIN
PATIENTS RELATED
CKD (eGFR <60 ml/min)
In particular in combination with:
 DIABETES
 AGE ≥ 75
PROCEDURE RELATED
 CHF (NYHA 3-4) and low LVEF
 CONTRAST ADMINISTRATION ROUTE (IA > IV)
 Acute myocardial infarction
 Contrast type (HOCM > LOCM/IOCM)
 Peripheral vascular disease
 Large doses of contrast medium
 Multi-vessel coronary disease
 Recent contrast administration (<72 h)
 Bypass graft intervention
 Hypertension
 Dehydration/low effective circulatory volume
 Baseline anemia (Hct <0.39 in male, <0.36 in female)
 Myeloma?
 Female gender?
 Rabdomyolysis
 Sepsis, cirrhosis
 Concomitant administration of nephrotoxic drugs
 Hemodynamic instability (peri-procedural hypotension, shock,
post-procedural blood loss, IABP)
 Need for cardiac surgery after CM exposure
 Metabolic disorders (hyperglycemia, hyperuricemia,
Toprak O (2013)
hypercolesteremia, metabolic syndrome, hypoalbuminemia)
Chronic Kidney Disease
Irrespective of causes, pre-existing
Chronic Kidney Disease
is the single most important
risk factor for CIN.
(both necessary and sufficient).
and the
associated incidence …
… increases in proportion with the severity of
baseline renal insufficiency.
35
30,6
7586 patients undergoing PCI
30
22,4
CIN, %
25
Data from
Minnesota Registry of
Interventional Cardiac
Procedures
20
15
10
5
2,4
2,5
<1,1
1,2-1,9
0
2,0-2,9
>3,0
Baseline SCr, mg/dl
Rinal CS et al., Circulation 2002; 105: 2259
Diabetes
Diabetes as
RISK MULTIPLIER
 It is not clear whether
diabetes ‘per se’ increases the
risk of CIN among patients with
normal renal function.
The coupling of diabetes with
CKD dramatically amplifies the
risk of CIN compared with that
observed for CKD of the same
degree without diabetes.
 Incidence among diabetic
patients has been reported to
be 9-40% in diabetic patients
with mild-moderate CKD and
>50% in those with severe CKD.
McCullough PA, JACC 2008; 51: 1419-1428
Advanced Age
 Some
studies indicate that
independent risk factor for CIN
advanced
age
is
an
Mehran et al., JACC 44: 1393-1399 (2004)
Marenzi et al., JACC 44: 1780-1785 (2004)
 … and some claims that this is not.
Rihal CS et al., Circulation 105: 2259-2264 (2002)
Meschi M et al., Crit Care Med 34: 2060-2068 (2006)
POSSIBLE REASONS:
 age related changes in renal structure and decline in renal function
(aging kidney)
 decline in endothelial function
 decreased antioxidant reserve
 reduced renal perfusion (renovascular disease, CHF, dehydration,
hemodynamic instability)
Route of administration (IA vs IV)
CIN incidence is significantly greater
in case of intra-arterial
administration (from 10-20% for
moderate to 25-70%
for high-risk patients)
compared to intravenous
administration (~5%)
Katzberg RW and Lamba R, Radiol Clin North Am, 47:789-800 (2009)
The higher risk of intra-arterial vs intra-venous administration.
Possible reasons:
 Higher doses of CM and higher concentrations of CM
reaching the kidneys
 More acute and direct exposure of the kidneys to CM
 Worse baseline ‘risk profile’
Published online: January 30, 2013
Comparison of Risks and Clinical Predictors of Contrast-Induced
Nephropathy in Patients Undergoing Emergency versus
Nonemergency Percutaneous Coronary Interventions
Chong E, Poh KK, Liang S, Soon CY, Tan HC
J Interven Cardiol 2010, 23(5): 451-459
STEMI
UA/NSTEMI*
WITHOUT MI*
(primary PCI)
(early PCI)
(elective PCI)
Overall
12.0
9.2
4.5
<0.0005
eGFR >60
8.2
9.2
4.3
<0.0005
eGFR 30-60
19.1
4.5
2.4
<0.0005
eGFR <30
34.4
40.0
25.9
0.510
P
*Pre-PCI saline hydration was given if baseline eGFR was <60 ml/min
The risk of CIN is significantly higher among STEMI patients. The most likely
contributing factors for CIN in this context are:
 impaired systemic perfusion caused by left ventricular dysfunction,
 the need for the administration of large volumes of CM,
 the lack of sufficient time to perform adequate pre-procedural hydration.
Accelerated prophylactic regimens can be considered in this cohort.
Clinical Evolution of CIN (1)
 Transient, usually mild, increase in serum creatinine within
the first 24-48 hrs post-contrast exposure.
 Usually non-oliguric.
 Urinalysis shows minimal or no proteinuria and bland
sediment with granular and epithelial casts and free renal
tubular epithelial cells.
 Low fractional excretion of sodium (<1%)
 Serum creatinine tipically peaks 3-5 days after the contrast
administration and returns to baseline or near baseline value
within 7-10 days in most cases.
 Where an acute change is detected, daily serum creatinine
measurements should continue until the peak is passed
Clinical Evolution of CIN (2)
In more severe cases (<15%), usually seen in people
with pre-existing CKD and diabetes:
 acute renal failure can occur in oliguric form
 oliguria typically persists for 2-5 days, occasionally
requiring temporary dialysis
 serum creatinine levels peak within 5-10 days and
return to baseline values within 14-21 days.
There is no effective therapy once
injury has occurred and
management is supportive.
PREVENTION
is crucial
given the short- and long-term
prognostic implications
associated to CIN
The development of CIN is associated with:
 Prolonged hospitalization and increased related costs
 Higher rates of in-hospital cardiovascular events
 Need for temporary dialysis (<1% to 6% according to
baseline renal function and patients’ risk profile)
 Persistence of residual renal dysfunction (~18%),
especially noted in patients with pre-existing CKD
 More rapid progression of underlying CKD to ESRD
requiring maintenance dialysis (<1%)
… and
… higher mortality rate!
35.7%
7.1%
1.1%
Serious Adverse Outcomes after
Contrast-Enhanced CT
Study
Tepel et al. (2000)
Becker & Reiser (2005)
Barrett et al. (2206)
Thomsen et al. (2008)
Kuhn et al. (2008)
Nguyen et al. (2008)
Weisbord et al. (2008)
TOTAL
CIN (%)
12.0
9.0
1.3
3.4
5.2
11.1
3.5
5.4
Dialysis
0/42
0/100
0/153
0/148
0/248
0/117
0/367
0/1175
Death
0/42
0/100
0/153
0/148
0/248
0/117
0/367
0/1175
NOTE – All studies were prospective and included patients with renal insufficiency,
with or without diabetes. Overall rate of CIN of 5.4%.
Katzberg RW and Newhouse JH, Radiology 2010; 256: 21-28
 Observational studies demonstrating a temporal
relationship between CIN and mortality could not
establish a cause-and-effect relationship.
 The comorbidities complicate and confound the
analysis: CIN may be simply a marker for increased
mortality risk rather than a contributing cause of death.
RECOMMENDATIONS
2. Before offering iodinated contrast agent to adults for nonemergency imaging, investigate for chronic kidney disease by
measuring eGFR.
Under 65 years old
Over 65 years old
Assess Risk of Renal Impairment
Measuring eGFR is a mandatory
requirement
• History of renal disease, proteinuria
• Prior kidney surgery
• Hypertension
• Heart or vascular disease
• Gout
• Diabetes Mellitus
If the answer to any of the
questions is YES, then measuring
eGFR is a mandatory requirement
Serum Creatinine → eGFR (CKD-EPI)
Must be obtained within 1 week of the examination for in-patients
Within 3 months for out-patients
Intravenous
Intra-arterial
<45 ml/min
<60 ml/min
No/Very Low risk* ≥45 ml/min
≥60 ml/min
At risk
*No specyfic prophylaxis or follow-up. Avoid dehydration.
Comment
The CMSC concludes that the risk of CIN is significantly lower following intravenous
CM administration. Evidence suggests that patients referred for contrast enhanced
CT are genuinely at risk of CIN if they have an eGFR <45ml/min
 WITHDRAWAL OF NEPHROTOXIC DRUGS AND METFORMIN
 CONTRAST MEDIUM USE
 PHARMACOLOGIC AGENTS
 HEMODIALYSIS/HEMOFILTRATION
 HYDRATION
Nephrotoxic medications to be witheld
before exposure to contrast media
 NON STEROIDAL ANTI-INFLAMMATORY DRUGS
 CALCINEURIN INHIBITORS
 LOOP DIURETICS
 MANNITOL
 AMINOGLYCOSIDES
 AMPHOTERICIN B
 VANCOMYCIN
 CHEMIOTHERAPEUTIC AGENTS
 ACE INHIBITORS & ANGIOTENSIN RECEPTOR BLOKERS
…
In patients with an eGFR <60 ml/min withdrawal of nephrotoxic
medications (at least 24 h before IV CM injection and 48 h before IA
administration) is considered best practice because these drugs in
combination with CM can have an additive injurious effect.
Metformin and intravenous contrast
Mark Otto Baerlocher MD, Murray Asch MD, Andy Myers MDCM
A DANGEROUS LIASON
 Metformin is not nephrotoxic per sé, but it is exclusively excreted by
the kidney.
 If contrast medium causes renal failure, metformin excretion is
reduced (up to 80%) and accumulation of the drug in the body occurs. In
this clinical setting, blood metformin levels may be many times greater
than the therapeutic level, potentially increasing the risk of lactic acidosis.
 8% of cases of metformin induced lactic acidosis occurs in the setting
of contrast induced nephropathy.
 Lactic acidosis has a mortality rate of up to 50%.
CMAJ January 8 2013: 185(1)
1) Patients with eGFR ≥60 ml/min/1.73 m2 can continue to take
metformin normally*
2) Patients with eGFR 30-59 ml/min/1.73 m2 receiving intra-arterial CM
should stop metformin 48 hrs before CM and should only restart
metformin 48 hrs after CM if renal function has not deteriorated
3) Patients with eGFR 30-44 ml/min/1.73 m2 receiving intravenous CM
should stop metformin 48 hrs before CM and should only restart
metformin 48 hrs after CM if renal function has not deteriorated
* Previous version (1999) recommended to stop metformin at the time of
injection in patients with normal renal function
Contrast Medium Use
Type of Contrast Medium
Meta-analysis of the relative nephrotoxicity of high- and low-osmolality
iodinated contrast media.
BJ Barrett and EJ Carlisle
Radiology 1993, 188: 171-178
OR* LOCM vs HOCM
Overall
0.61 (95% CI 0.48-0.77)
Patients with prior renal failure
0.50 (95% CI 0.36-0.68)
Patients without prior renal failure
0.75 (95% CI 0.52-1.10)
*Odds Ratio of a rise in SCr level of >0.5 mg/dl
Data from 25 trials
Favors IOCM
Favors LOCM
NS
Data from 36 RCTS. Overall 7,166 pts (3,672 iodixanol; 3,494 LOCM )
 Iodixanol-associated reduction suggestive for a lower incidence of
CIN, but statistically not significant
 Incidence of CIN significantly lower with iodixanol when compared
with iohexol (OR 0.25, 95% CI 0.11-0.55, P <0.001) but not when
compared with LOCM other than iohexol (OR 0.88, 95% CI 0.70-1.10,
P=0.25)
 Analysis of patient subgroups revealed no significant difference in
the incidence of CIN with iodixanol vs LOCM among patients
 receiving intra-arterial CM injections
 with and without diabetes and/or renal insufficiency
 undergoing coronary angiography with or without PCI
Contrast Medium Use
Type of Contrast Medium
Volume and Frequency of Administration
Searchin’ for the ‘Magical’ volume
Maximum Contrast Dose (MCD) ≤100 ml
Davidson CJ et al., Ann Intern Med 1989; 110: 119-124
MCD = (5 x body weight [kg] / SCr [mg/dl])
Cigarroa RG et al., Am J Med 1989; 86: 649.652
Freeman RV et al., Am J Cardiol 2002; 90: 1068-1073
CM volume [ml] / CCr [ml/min] ratio <3.7
Laskey WK et al., J Am Coll Cardiol 2007,50: 584-590
g-I iodine [grams] / eGFR [ml/min/1.73 m2] ratio ≤1
Nyman U et al, Acta Radiol 2008; 49: 658-667
CM volume [ml] / MCD ratio <1
Marenzi G et al., Ann Intern Med 2009; 150: 170-177
MCD <4 ml/kg
Wijns W et al., Eur Heart J 2010; 31: 2501-2505
CM volume [ml] / eGFR [ml/min/1.73 m2] ratio <2.39
Liu Y et al., Int Urol Nephrol 2012, 44: 221-229
A ‘safe’ volume does not exist. Even doses as low as 20 to 30 ml are
capable of inducing CI-AKI in high risk patients.
Thus …
 In all patients only the minimum amount of contrast medium
necessary to answer the clinical diagnostic question should be used
 It is often possible to dilute CM further with normal saline without
affecting image quality.
Moreover
 Repeated exposure should be delayed for 48 in patients without
risk factors and 72 h in those with diabetes or pre-existing CKD.
 Ideally, the interval between procedures should be 2 weeks, the
expected recovery time of the kidney after acute injury.
Pharmacological Prophylaxis
Background
The mechanisms of pharmacological prophylaxis for CIN include
antioxidant strategy, inhibition of renal vasoconstriction, and
combination of these two effects.
CONTRAST MEDIA
DIRECT TOXICITY TO
PROXIMAL
TUBULAR CELL
Vasopressin
release
HEMODYNAMIC EFFECTS
Statins
Osmolality related
Osmotic
diuresis
Adenosine
release
Theophylline
TUBULAR INJURY
Vacuolization
Necrosis
Apoptosis
Tubular obstruction
…
Furosemide
ET receptor
antagonists
(tubulo-glomerular feedback)
Distal sodium delivery
O2 consumption
due to sodium
reabsorption
O2 free-radicals generation
and release
RHEOLOGIC EFFECTS
Furosemide
Mannitol
Endothelial dysfunction
Viscosity related
Endothelin
release
Blood
viscosity
Tubular fluid
viscosity
L-Arginine
Tubular luminal
PGE1 dilatation
and
tubular-interstitial
Statins
pressure
Nebivolol
VASOCONSTRICTION
NO and PGs
synthesis
Reactivity to
Angio II
Reduced medullary blood flow
CCB, ANP Urine
Dopamine flow rate
Fenoldopam
Altered renal microcirculation
ACEi
MEDULLARY ARB
HYPOXIA
N-acetylcysteine
Allopurinol
Ascorbic acid
ACUTE RENAL FAILURE
Statins, Nebivolol
Renal CM
retention
Decreased GFR
20
10
%
HR = 0.97
%
16
8
12,7
12,7
12
6
Est
Est
8
4
4
2
0
0
NAC
Placebo
Primary end point (incidence of CIN)
NAC
Placebo
Combined end point
(mortality/need for dialysis at 30 days)
2308 pts, At least 1 risk factor (>70 yrs, CKD, diabetes, CHF, LVEF <0.45, hypotension)
NAC (1172 pts) 1200 mg po BID pre and post study vs Placebo (1136 pts)
Hydration: NS 1 ml/kg/h 6-12 hrs pre/post-study
Oral Statins for CIN Prevention
The rationale for Statins use for the prevention of
CIN relates to its:
 antioxidant and anti-inflammatory properties
 capacity of improving endothelial function
Weisbord SD and Palevsky PM
Curr Opin Nephrol Hypertens 2010, 19: 539-549
Pre-procedural use of statins leads to a significantly reduction (46%)
in the pooled risk for CIN (RR 0.54, 95% CI 0.38-0.78, p <0.001)
No drugs have been approved by the regulatory authorities
for the prevention of CIN and the CMSC did not support
pharmacological prophylaxis for preventing CIN because
none of the pharmacological manipulations has been
shown to offer consistent protection.
Renal Replacement Therapies
Background
Contrast media can be efficiently removed from blood by intermittent
hemodialysis, and a single session effectively removes 60 to 90% of
contrast media.
Yet, reduction of CIN with dialysis is not biologically plausible since
the CM would reach the kidneys within one or two cardiac cycles and
subsequent removal of CM is unlikely to stop the cascade of renal
injury, which would have already begun.
KDIGO comment. The effective removal of creatinine during HF or IHD makes it difficult to be certain
that the observed lower incidence of CI-AKI is not related to transport removal of creatinine during
the procedure.
25
24
RCIN, %
Nine randomized
trials and 2 nonrandomized trials
were included; 8
studies used HD
and 2 used HF or
HDF.
RR=1.02
23,3
23
22
21,2
21
20
RRT
SMT
CLINICAL SIGNIFICANCE
Despite effective CM removal, RCIN occurred at
an equal or higher rate in patients undergoing
periprocedural RRT than in control patients.
4.5.1
We suggest not using prophylactic intermittent hemodialysis (IHD) or
hemofiltration (HF) for contrast media removal in patients at
increased risk for CI-AKI.
And the Oscar goes to …
Hydration and Volume Expansion
Background
Volume expansion by adequate hydration is the single most important
measure that can be taken prior to intravascular CM administration.
All patients considered at risk for CIN should be fluid loaded.
ADEQUATE VOLUME EXPANSION …
 Promote diuresis
 Dilute CM in the tubules thus attenuating its direct toxic effect on
the tubular cells
 DIminishes fluid viscosity in the tubules and vessels with
subsequent improved microcirculation
 Attenuates the vasoconstrictive effect of CM on renal medulla
and increases renal production of endogenous vasodilator, thus
increasing regional blood flow
PERI-PROCEDURAL FLUID ADMINISTRATION PROTOCOLS
IV FLUID
1) 0.9% NaCl @ 1.0-1.5 ml/kg/hr for 12 hr pre and for 12 hr post CM administration
for same day administration
2) Isotonic NaCl or NaHCO3 @ 3 ml/k/hr for 1-3 hr pre and for 6 hr post CM
administration
or
3) Isotonic NaHCO3 @ 3 ml/kg/hr for 1 hr pre and @ 1 ml/kg/hr for 6 h post CM
administration
 The aim is to achieve a ‘good’ urine output (>150 ml/h) in the 6 hrs after the
radiological procedure.
Consensus Guidelines for the Prevention of Contrast Induced Nephropaty
Isotonic bicarbonate vs. normal saline
1) SODIUM BICARBONATE: PROS
 Antioxydant effects
 Anti-inflammatory properties
2) NORMAL SALINE: CONS
 Chloride load
Review and meta-analysis of 18 prospectively randomized studies.
CI-AKI occurred in 11.5% of 3,055 study patients.
 Use of sodium bicarbonate provided an overall benefit for prevention of CIAKI with bordeline statistical significance (RR = 0.66, 95% CI = 0.45-0.95, P =
0.03)
 Bicarbonate therapy was most effective in coronary procedures, especially
when emergent (RR = 0.13, 95% CI = 0.04-0.42, P = 0.0007)
 Bicarbonate therapy showed a borderline significant trend for benefit in
patients with CKD (RR = 0.66, 95% CI = 0.44-1.01, P=0.05)
 There was no effect on need for RRT or mortality
The relative low quality of the individual studies, heterogeneity and
possible publication bias means that only a limited recommendation
can be made in favour of the use of sodium bicarbonate.
Hydration with sodium bicarbonate for the prevention of contrastinduced nephropathy: a meta-analysis of randomized controlled trials
H. Trivedi1, R. Nadella1 and A. Szabo2
1Division of Nephrology and 2Department of Population Health, Medical College of Wisconsin,
Milwaukee, WI, USA
Ten randomized comparisons of isotonic sodium bicarbonate vs normal sodium
chloride entered analysis (total = 1,090)
OR bicarbonate vs chloride
Overall
0.57 (95% CI: 0.38-0.85)
Study without additional prophylactic agents
0.33 (95% CI: 0.17-0.62)
No evidence of heterogeneity (P=0.10) and no publication bias (P=0.34)
CONCLUSIONS
The summary effect of randomized trials favors hydration with
sodium bicarbonate for the prevention of contrast-induced
nephropathy
Clinical Nephrology 2010, 74(4): 288-296
Hydration regimens using isotonic sodium bicarbonate or normal saline
may be employed and there is probably no difference between the two fluid
regimens
Canadian Association of Radiologists, 2011
The Committee considers that there is enough evidence to recommend that
either volume expansion regimen may be used.
The sodium bicarbonate protocol is quicker than the optimal sodium
chloride regimen and may be useful for outpatients
Updated ESUR Contrast Media Safety Committee Guidelines, 2011
Data on the comparative effectiveness of bicarbonate and saline for the
prevention of CIN are insufficient to warrant a recommendation for the
routine use of a specific isotonic intravascular fluid.
NHS, National Clinical Guideline Center, 2013
Some studies and meta-analyses have shown hydration with sodium
bicarbonate to be superior to 0.9% saline in reduction the risk of CIN, but
these results have been challenged by other meta-analyses and cannot be
considered definitive at this time.
ACR Committee on Drugs and Contrast Media (Version 9), 2013
COMMENT
The role of oral hydration to prevent CIN continues to evolve. Its potential
efficacy seems promising if suplemented with oral sodium chloride. At
the present time, the evidence base is not sufficiently robust to
recommend oral fluid prophylaxis alone as a surrogate of iv hydration.
RenalGuard SystemTM
RenalGuard System™ is comprised of a urinary
collection bag that is hung on a digital scale that
in turn drives a high volume fluid pump. Each
drop of urine entering the collection bag results
in an equal volume of saline infused back into the
patient. The infusion rate is adjusted second by
second in response to changes in urine output,
thus preventing a net loss or gain of fluid from
the body.
By administering a small bolus of normal saline
initially (~3 ml/kg over 20-30 min) and initiating
diuresis with a small dose of furosemide (0.25
mg/kg iv), urine output increases to 500-600 ml/h
in about 60 min and can be sustained for 6 h
usually without additional diuretic administration.
The patient is given the contrast agent when urine
output exceeds 300 ml/h. The matching of urine
output with intravenous fluid input continues
throughout the procedure and for 4 h after the
completion of angiography.
Given the high urine rate per hour, it is necessary
to have a Foley catheter in place.
P=0.003
RR=0.16
95% CI 0.04-0.58
OR = 0.47, 95% CI 0.24-0.92
P = 0.025
P=0.005
RR=0.29
95% CI 0.10-0.85
30/146
P=0.44
RR=0.42
95% CI 0.10-1.82
16/146
Overall
Elective
Urgent
angiography angiography
Recommendations to PREVENT CI-AKI:
 Confirm the need for contrast media
 Identify the high-risk patient (assess baseline eGFR!)
 Discontinue nephrotoxic drugs before the procedure
 Hydrate adequately
 Use the lowest possible volume of low-osmolar or isoosmolar contrast media and avoid repeated injection
 Check eGFR 24 - 48 and 72 hours after study
CONCLUSION
Contrast-Induced Nephropathy is
likely to remain a significant
challenge in the future because
the patient population is aging
and chronic kidney disease and
diabetes are becoming more
common.
Peter A. McCullough (2008)