Open Journal of Anesthesiology, 2013, 3, 421-426
Published Online November 2013 (http://www.scirp.org/journal/ojanes)
http://dx.doi.org/10.4236/ojanes.2013.39088
Open Access OJAnes
421
Renal Function after Coronary Artery Bypass Graft Using
Dexmedetomidine
Alexandre Fabricio Martucci1, Yara Marcondes Machado Castiglia2
1Ponta Grossa State University, Ponta Grossa, Brazil; 2Botucatu College of Medicine, Botucatu, Brazil.
Received September 18th, 2013; revised October 19th, 2013; accepted November 2nd, 2013
Copyright © 2013 Alexandre Fabricio Martucci, Yara Marcondes Machado Castiglia. This is an open access article distributed under
the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.
ABSTRACT
Acute kidney injury (AKI) is defined by 0.3 mg/dL increase in serum creatinine (SCr) and is associated with higher
incidence of postoperative mortality after coronary artery bypass graft (CABG). There are few clinical studies on the
effect of dexmedetomidine (DEX) on renal function. We evaluated AKI after coronary artery bypass graft with and
without cardiopulmonary bypass (CPB) under anesthesia with DEX. Method: In this retrospective study, we performed
serial analysis of serum creatinine (SCr) up to 48 hours after surgery in 286 patients who underwent CABG. We tested
the similarity between groups, evaluating patients separately for use of CPB and DEX. Each patient was evaluated for
his or her SCr at the following points in time: preoperative, immediately postoperative, 24 hours postoperative, and 48
hours postoperative. Preoperative SCr was used as the baseline value for each patient. If the SCr increased ≥0.3 mg/dL
in at least one of the periods, the patient was classified as having AKI. We also assessed the risk for AKI in patients
with altered preoperative SCr (values between 1.1 to 2.0 mg/dL for women or 1.3 to 2.0 mg/dL for men) compared to
patients with normal SCr. Results: The groups were similar for preoperative weight, age, and altered SCr. Patients were
anesthetized with DEX and who underwent CPB exhibited higher incidence of AKI (p = 0.043). Without CPB, there
was higher incidence of AKI after using DEX (p = 0.066). Conclusion: Anaesthesia with DEX increased the incidence
of AKI after myocardial revascularization surgery in patients who underwent CPB.
Keywords: Acute Kidney Injury; Dexmedetomidine; Cardiopulmonary Bypass; Coronary Artery Bypass Graft
1. Introduction
Acute kidney injury (AKI) [1,2] is defined by 0.3 mg/dl
increase in serum creatinine (SCr) and is associated with
higher incidence of postoperative mortality after myo-
cardial revascularization surgery [3-7]. As indicated by
its pathophysiology, AKI has multifactorial causes, in-
cluding low cardiac output, hypoperfusion, hypovolemia,
diabetes mellitus, age ≥ 65 years old, emergency surgery,
renal ischemia, use of cardiopulmonary bypass (CPB),
and adopted rewarming method after CPB [7-15]. There
is 30% incidence of AKI in patients undergoing myocar-
dial revascularization and approximately 1% will require
dialysis [7,8,16].
Dexmedetomidine (DEX) is an α2-adrenoceptor ago-
nist with α2/α1 selectivity of 1600:1. Doses between 0.2 -
0.6 µg/kg/h promote sedation, anxiolysis, hypnosis, and
analgesia with little or no change in breathing [17]. DEX
acts on three types of α2 receptors (A, B, and C). The α2A
has been described in the periphery and α2B and α2C in the
central nervous system (CNS). In the periphery, the pre-
synaptic receptors inhibit noradrenaline release, while
post-synaptic receptors determine vasoconstriction. DEX
acts on central receptors, causing sympatholysis, sedation,
and antinociception [18]. In the cardiovascular system,
DEX reduces heart rate, peripheral vascular resistance,
and indirectly, myocardial contractility, cardiac output,
and systemic pressure. Incidences of bradycardia and
hypotension have been associated with loading dose.
Under anesthesia, DEX drastically reduces the minimum
alveolar concentration (MAC) [19]. In cardiac surgery,
DEX reduces catecholamine plasma concentrations,
maintains hemodynamic stability, and increases urinary
output [20]. Despite maintaining antidiuretic hormone
(ADH) concentration, another α2 agonist, clonidine, in-
creases diuresis and creatinine clearance on the first night
after surgery [21]. Thus, with respect to renal function,

Renal Function after Coronary Artery Bypass Graft Using Dexmedetomidine 422
DEX may be a promising agent for use in myocardial
revascularization surgery. Therefore, we conducted a
retrospective study to assess the effect of using DEX in-
traoperatively on postoperative renal function in patients
who underwent myocardial revascularization surgery with
and without CPB.
2. Methods
This retrospective study was approved by the appropriate
ethics authority (Ref: 120/2011) and registered with
REBEC (Ref: U1111-1128-4201). Written informed con-
sent was waived by the ethics committee. We selected pa-
tients who underwent anaesthesia for myocardial revas-
cularization between January 2008 and December 2011.
We excluded patients who met the following exclusion
criteria: underwent emergency surgery and catheteriza-
tion within less than 72 hours before the operation, had
≥2 mg/dl serum creatinine (SCr) before surgery, had in-
complete data, and patients with continued use of α2 ago-
nist. Patients were divided into the following groups
based on use of CPB and DEX:
Group G(CPB)—CPB patients
Group G(Control)—non-CPB patients
Group G(CPB + DEX)—CPB patients who received DEX
Group G(DEX)—non-CPB patients who received DEX
For G(CPB) and G(Control), the anesthesia protocol began
with 3 to 5 mg of intravenous midazolam. Standard ASA
monitors were attached, and radial artery catheterization
was used for monitoring mean arterial pressure. We in-
jected 20 to 30 μg/kg fentanyl, 0.3 mg/kg etomidate, and
0.08 mg/kg pancuronium. Anaesthesia was maintained
by isoflurane titration according to hemodynamic respon-
se using 60% O2 as carrier. Mean arterial pressure was
maintained between 60 and 90 mmHg. We used meta-
raminol or ephedrine for short episodes of hypotension,
noradrenaline for episodes of low peripheral vascular re-
sistance, dobutamine to increase cardiac inotropism, and
sodium nitroprusside or nitroglycerin for hypertensive
crisis.
For G(CPB+DEX) and G(DEX), we used DEX at 0.5 µg/
kg/h dose immediately after venipuncture and monitoring
without loading dose, then reducing the fentanyl dose to
10 to 20 μg/kg. Use of isoflurane and vasoactive agents
was kept the same as for G(CPB) and G(Control).
To start CPB, the patients were anticoagulated with so-
dium heparin (4 mg/kg) or until reaching activated clot-
ting time (ACT) higher than 480 seconds. During CPB,
nonpulsatile flow was used with target mean arterial
pressure from 50 to 80 mmHg. Temperature was meas-
ured with a nasopharyngeal thermometer and maintained
between 30˚C and 35˚C during CPB.
To quantify AKI rates in patients who underwent
CABG with and without CPB, we used the results from
tests routinely performed at the following time points:
preoperative (Mpre), immediately postoperative (MiPO), 24
hours postoperative (MPO24), and 48 hours postoperative
(MPO48). These data were collected by reviewing elec-
tronic records available in the TASY® program, version
2.6, developed and licensed by Whebsistemas. The fol-
lowing were used as criteria to define AKI: AKIN (Acute
Kidney Injury Network), ≥0.3 mg/dl increase in SCr
concentration, or ≥50% increase in SCr concentration
from baseline within at least 48 hours without urine out-
put analysis [1]. Each patient was evaluated for SCr con-
centration at time points starting from Mpre. The SCr
concentration at each time point was compared to that in
Mpre. If at least one of these comparisons between time
points indicated ≥0.3 mg/dl increase in SCr concentration,
the patient was classified as having AKI. We also as-
sessed risk for AKI in patients with altered preoperative
SCr (values between 1.1 mg/dl and 2.0 mg/dl for women
or 1.3 mg/dl and 2.0 mg/dl for men) compared to patients
with normal SCr.
The statistical analysis aimed to test whether there was
significant difference in incidence of AKI when using
DEX, thus we separated patients who underwent CPB
from those who did not. We considered Student t-test for
independent samples in comparing two groups with re-
spect to quantitative variables. We considered Fisher
exact and Chi-square tests in assessing the association
between qualitative variables. Values were considered
statistically significant at p < 0.05.
3. Results
We evaluated 543 patients, of whom 257 patients were
excluded because they met the exclusion criteria. A total
of 286 patients were included in the statistical study, dis-
tributed as follows: GCPB, 157 patients; GCPB + DEX, 50 pa-
tients; Gcontrol, 55 patients; and GDEX, 24 patients.
We confirmed similarity between groups for weight,
age, preoperative SCr, and incidences of hypertension
(HTN) and diabetes mellitus (DM) preoperatively, for
samples with and without CPB (see Tables 1 and 2).
Analysis of the results tested if there was some other
factor associated with the AKI studied. Among the
groups that underwent CPB or not, we separately tested
weight, age, and altered preoperative SCr concentration
up to 2 mg/dl. For those patients who did not undergo
CPB and received DEX or not, only age (p = 0.008), but
not weight (p = 0.912) or altered SCr (p = 0.488), was
associated with higher incidence of AKI. Incidence of
AKI was higher in the group that received DEX, even in
patients who did not undergo CPB, but without statistical
significance (p = 0.066) (Figure 1).
For groups that underwent CPB, the DEX factor was
associated with a higher incidence of AKI (p = 0.043;
beta error of 0.273) (Figure 2). In these patients, age (p =
0.224), weight (p = 0.067), and altered SCr up to 2 mg/dl
Open Access OJAnes

Renal Function after Coronary Artery Bypass Graft Using Dexmedetomidine
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423
Table 1. Testing similarity of the groups that were submitted to CPB and that received or did not receive DEX, for weight,
age, and altered preoperative serum creatinine concentration up to 2 mg/dl.
Variable DEX n Mean Median Minimum Maximum Standard deviation p-value*
Without 157 64.0 64.0 36.0 87.0 9.0
Age
With 50 64.4 65.0 39.0 82.0 9.8
0.755
Without 157 74.7 73.0 45.0 116.0 13.4
Weight
With 50 72.8 72.5 44.0 97.0 11.7
0.347
Without 157 1.20 1.18 0.63 1.98 0.28
Altered Pre-Op.
Creatinine With 50 1.14 1.15 0.72 1.60 0.24
0.171
*Student t-test for independent samples.
Table 2. Testing similarity of the groups that were not submitted to CPB and that received or did not receive DEX, for weight,
age, and altered preoperative serum creatinine concentration up to 2 mg/dl.
Variable DEX n Mean Median Minimum Maximum Standard deviation p-value*
No 55 61.8 65.0 34.0 85.0 11.9
Age
Yes 24 65.5 67.0 48.0 78.0 7.2
0.097
No 55 73.8 73.0 47.0 119.0 13.8
Weight
Yes 24 73.2 72.5 40.0 101.0 15.7
0.862
No 55 1.11 1.10 0.68 1.92 0.28
Alt. Pre-Op.
Creatinine Yes 24 1.08 1.13 0.71 1.44 0.23
0.649
With DEX Without DEX
16.7%
3.6%
%
35
30
25
20
15
10
5
0
With DEX Without DEX
32%
18.5%
%
35
30
25
20
15
10
5
0
Figure 2. Percentage of acute kidney injury cases in patients
who were submitted to CPB according to DEX use (p =
0.043; beta error of 0.273).
Figure 1. Percentage of cases with acute kidney injury (AKI)
according to DEX use in patients who were not submitted
CPB (p = 0.066; beta error of 0.831).
creased incidence of AKI in the non-CPB group, as ex-
pected for changes associated with aging [13,22]. Al-
though, age is not necessarily a risk factor, other studies
corroborate the results found for the non-CPB group
[3-7].
(p = 0.364) exhibited no statistically significant associa-
tion with AKI.
4. Discussion
In this study, we found higher incidence of AKI in
groups that received DEX regardless of CPB use. We
also observed similarity for preoperative creatinine, sex,
age, weight, and incidence of HTN and DM in the sam-
ple studied, further validating the results of this retro-
spective study. The age factor was associated with in-
SCr is a late biomarker of AKI. Although other bio-
markers, such as KIM-1 (Kidney Injury Molecule), NAG
(N-acetyl-B-D-glucosaminidase), NGAL (Neutrophil Ge-
latinase Associated Lipocalin), IL-18 (Interleukin 18), or
cystatin C seem promising, the present definition of AKI
is still based on altered serum creatinine concentration

Renal Function after Coronary Artery Bypass Graft Using Dexmedetomidine 424
and urine output [23-25]. Urinary output can increase the
sensitivity for diagnosing AKI, but as this parameter is
used to determine the phase of AKI, very constant meas-
urements are required, which poses considerable diffi-
culty in clinical practice [26]. Current clinical practices
do not emphasize small SCr increases, which are often
attributed to laboratory variation. However, the coeffi-
cient of variation of SCr with modern analyzers is rela-
tively small and therefore 0.3 mg/dL increases are un-
likely to be caused by laboratory variation [27]. Accord-
ing to Tolpin and colleagues [5], even subclinical in-
creases are associated with worse prognosis. However,
there is an overall consensus that diagnostic criteria should
only be applied when optimal hydration status has been
established [1].
CPB is an AKI-independent risk factor in renal func-
tion after myocardial revascularization surgery. The
causes contributing to CPB as a risk factor are still being
studied, but several factors have been proposed, such as
hypothermia and rewarming, oxygen delivery to the kid-
neys (renal DO2), perfusion method employed, perfusion
pressure, and CPB duration itself [4,6,10,14,15,28,29].
Each factor would partially contribute to some kind of
injury. Because the SCr values obtained before surgery
are similar enough among all patients studied, this could
emphasize intraoperative factors as probable determi-
nants of AKI, including use of CPB and DEX.
Kulka and colleagues [21] studied preoperative treat-
ment of patients undergoing myocardial revascularization
with clonidine (4 µg/kg intravenously) and believe that
this other agonist α2 prevented renal function deteriora-
tion in patients, probably by reducing the sympathetic
nervous system response. These authors’ conclusion was
based on studying creatinine clearance in patients treated
with agonist α2 compared to creatinine clearance in un-
treated patients. At three days after surgery, the clear-
ances of the two groups were equal. However results
from additional clinical trials are still necessary.
An in vitro experiment with human kidney cells and in
vivo experiment with mice demonstrated that DEX acti-
vates the cell survival signal, phosphorylated AKT anti-
body (pAKT) via α2 adrenoceptors, to reduce cell death
and release the nuclear protein HMGB1 (high mobility-
group box-1) in the plasma, inhibiting TLR4 (toll-like
receptor 4) signaling, where both HMGB1 and TLR4
determine renal protection and play a central role in co-
ordinating inflammatory responses in renal ischemia and
reperfusion. DEX also has protective properties for or-
gans as well as cytoprotective and anti-inflammatory ef-
fects, protecting against renal injury after ischemia and
reperfusion. The authors of the study believe that, if ex-
trapolated to clinical practice, their results indicate that
DEX determines renal protection against ischemia and
reperfusion injuries [30].
In contrast, other authors of histological studies found
that using DEX in rats caused dilation, degeneration, and
necrosis of renal tubules after hemorrhage of 30% of
volemia, without replacing this loss. However, there was
reduced renal vascular resistance in organ function, with
increased glomerular filtration and renal filtration frac-
tion [31].
In this retrospective study it was not possible to obtain
a precise conclusion due to the sample size. Missing data,
emergency surgeries, and other exclusion criteria left us
with a small sample, especially for the non-CPB group.
However, we found that DEX increased the incidence of
AKI in the CPB group. In patients without CPB use, DEX
was not considered an independent risk factor for AKI
because p-value was 0.066, which would only indicate a
statistically significant trend with a larger sample power.
Thus, more patients are probably necessary to demon-
strate if DEX is also a risk factor for AKI in patients not
undergoing CPB.
5. Conclusion
In conclusion, albeit with a small sample, we observed
that DEX behaved as an independent risk factor for in-
creased incidence of AKI after CABG in patients who
used CPB. For the non-CPB group, our sample was too
limited to reach a conclusion.
6. Acknowledgements
Mr. Ary Elias Sabbag Jr., for his help with statistical ana-
lysis.
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