Open Journal of Anesthesiology, 2013, 3, 356-362
http://dx.doi.org/10.4236/ojanes.2013.38076 Published Online October 2013 (http://www.scirp.org/journal/ojanes)
Renal Function after Major Uro-Oncologic Surgery and
Dexmedetomidine Infusion
Marcus Vinicius M. Novaes1, Paulo Sergio G. Lavinas1, Grace Haber D. Pires1,
Ana Claudia G. de Carvalho1, Renata M. B. Lopes1, Regina El Dib2, Paulo do Nascimento Jr.2
1Cancer Institute (INCA), Rio de Janeiro, Brazil; 2Department of Anesthesiology, Univ Estadual Paulista (UNESP), Botucatu, Brazil.
Received August 2nd, 2013; revised September 2nd, 2013; accepted September 19th, 2013
Copyright © 2013 Marcus Vinicius M. Novaes et al. This is an open access article distributed under the Creative Commons Attribu-
tion License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
ABSTRACT
Obje ctive: Acute kidney injury in major surgery is associated with increased postoperative mortality. This study aimed
to evaluate renal function after major urologic surgery and intraoperative dexmedetomidine infusion. Methods: Thirty
oncologic patients with normal renal function scheduled for prostatectomy or nephrectomy, anesthetized with combined
epidural and general anesthesia, were randomized to receive either intraoperative blind infusion of dexmedetomidine
(Dexmedetomidine Group, n = 15, 0.5 μg/kg load dose plus 0.7 μg/kg/h) or 0.9% saline (Control Group, n = 15) until
the end of surgery. Intraoperative and cumulative 24-hour diuresis, serum creatinine (SCr), calculated creatinine clear-
ance (ClCr) and serum cystatin C (SCys) at postoperative days 1, 2 and 3 and 2 weeks after surgery were evaluated. Re-
sults: Mean ± standard deviation values for intraoperative diuresis in Dexmedetomidine and Control Groups were 566
± 396 mL and 298 ± 153 mL, respectively (p = 0.014). Cumulative 24-hour diuresis in Dexmedetomidine and Control
Groups was 1947 ± 266 mL and 1748 ± 237 mL, respectively (p = 0.91). Mean values of SCr, ClCr and SCys were not
significantly different from their baseline values in both groups and no significant differences were seen between
groups at any moment for two weeks (p > 0.05). Conclusion: According to the doses used in this study, despite an in-
traoperative increase in diuresis, intraoperative infusion of dexmedetomidine did not influence renal performance up to
two weeks after major uro-oncologic surgery, as evaluated by SCr, ClCr and SCys.
Keywords: Dexmedetomidine; Renal Function; Nephrectomy; Prostatectomy; Epidural; General Anesthesia
1. Introduction
Acute kidney injury (AKI) is usually seen in the pe-
rioperative period, mainly after major surgeries [1]. It has
been observed that postoperative elevated values of se-
rum creatinine are associated with increases in time and
cost of hospital stay and with high rates of morbidity and
mortality [2]. Urological procedures are considered to be
of high risk for the development of perioperative kidney
injury [3], and nephrectomy has the highest potential to
cause AKI [4].
Several strategies are used to either prevent or mini-
mize perioperative AKI. These can be either pharmacol-
ogical or nonpharmacological strategies, even involving
early dialysis techniques [5]. Dexmedetomidine, an α2-
agonist drug with sedative, analgesic, and diuretic prop-
erties [6], has been assessed in the protection of organs
such as brain, heart, and kidneys and conflicting results
have been obtained [7-9]. No drug, alone or in combina-
tion, was shown to be effective in preventing periopera-
tive AKI until the present time [7].
In the present study, to test the hypothesis that dex-
medetomidine enhances postoperative renal performance,
its potential to increase diuresis and creatinine clearance
was evaluated in major urologic surgery.
2. Methods
This prospective and randomized study was approved by
the Institutional Review Board of the National Cancer
Institute, Rio de Janeiro, Brazil. Thirty patients sched-
uled for nephrectomy or prostatectomy at the National
Cancer Institute (Rio de Janeiro, Brazil), signed the In-
formed Consent and were included in the study. The fol-
lowing criteria were filled for the patients to be included
in the study: American Society of Anesthesiologists

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 357
(ASA) physical status 1 - 2 of both sexes; age, 30 - 65
years; height, 1.50 - 1.90 m; no history of renal dysfunc-
tion; serum creatinine ≤ 1.3 mg/dL; and no contraindica-
tion to epidural block. Patients using diuretics and/or
clonidine were excluded from the study.
All patients received diazepam, 10 mg, oral route, the
night before surgery. In the operating room, patients
were monitored (Datex Ohmeda Aespire, PSVPro inside,
Madison, USA) with continuous electrocardiography,
bispectral index, invasive blood pressure (by radial artery
catheterization), pulse oximetry, and capnography, the
latter after tracheal intubation. A large-bore peripheral
intravenous (IV) line was inserted in the upper limb and
a 500 mL bolus of lactated Ringer’s solution was infused
followed by a 8 mL/kg/h infusion throughout the surgery.
Central venous access was also obtained after tracheal
intubation.
Patients were then randomly divided into two groups
for blind infusion of dexmedetomidine (Dexmede-
tomidine Group, n = 15), 0.5 µg/kg in 20 minutes fol-
lowed by an infusion of 0.7 µg/kg/h until the end of sur-
gery; or 0.9% saline (Control Group, n = 15), with the
same infusion protocol until the end of surgery. An Anne
infusion pump was used (Anne; Abbott, Abbott Park,
USA) and the solutions were prepared by a person not
involved in the anesthetic-surgical procedure. After ini-
tial bolus of solution in study, epidural anesthesia was
induced with the patient in lateral decubitus, between the
L2 and L3 segments and a fixed dose of 0.75% ropiva-
caine, 20 mL, with morphine, 2 mg, was injected in all
patients. General anesthesia was induced 20 minutes af-
ter epidural injection with target-controlled infusion (TCI)
of propofol (3.0 - 4.0 µg/mL), neuromuscular blockade
was achieved with cisatracurium (0.2 mg/kg) and tra-
cheal intubation was preceded by administration of lido-
caine, 1.5 mg/kg IV. Anesthesia was maintained with
TCI propofol and cisatracurium as needed.
If a decrease greater than 30% of baseline occurred in
the values for mean arterial pressure or a systolic blood
pressure less than 80 mmHg was present, administration
of a 300 mL bolus of 6% hydroxyethyl starch solution
(HES, mean molecular weight, 130 kDa; degree of sub-
stitution, 0.4) would be performed and could be repeated.
Bradycardia was defined as a heart rate lower than 45
beats per minute and would be treated with atropine, 0.5
mg IV. Administration of packed red blood cells (pRBC)
was established if the hematocrit value was below 25%.
If the values for the mean arterial pressure continued
lower than the limits defined in the study even after vo-
lume replacement (HES and/or pRBC), administration of
adrenaline, 2 - 4 g/min, would be performed and the
administration of solution in study could be interrupted.
Other perioperative parameters included length of
surgery, volume and type of liquids administered, and
adrenaline use in the operating room and post anesthesia
care unit (PACU).
Diuresis was evaluated on a cumulative basis in the
intraoperative period and 4, 12, and 24 hours after sur-
gery. At the first three postoperative days and two weeks
after surgery, renal function was assessed by the values
for serum creatinine (SCr) and creatinine clearance (ClCr)
by using the Cockroft-Gault equation [10]. Additionally,
renal function was also assessed by the values for serum
cystatin C (SCys) in the same moments.
Recording of hemodynamic variables was made at the
following times: baseline (right after patient monitoring);
10 and 20 minutes after infusion of the study solution
was initiated; 20 minutes after epidural blockade (before
induction of general anesthesia); after tracheal intubation;
immediately before surgical incision; after start of sur-
gery; end of surgery; 1 and 2 hours after admission of the
patient in PACU; and discharge from the PACU.
Statistical Analysis
The number of participants in this study was calculated
from the difference observed in the clearance of postop-
erative creatinine after intraoperative administration of
dexmedetomidine as compared to the group not receiving
the drug, according to Frumento’s study [11]. A mini-
mum of 24 patients (divided into two randomized groups)
was necessary for a statistical power of 80% with α =
0.05. Continuous variables were presented as mean ±
standard deviation (SD) and compared with the Student’s
t test. Variables with high variability were compared us-
ing the Mann-Whitney test. The chi-square test was used
in proportions. Continuous variables were analyzed with
ANOVA followed by the Bonferroni test when appropri-
ate. For all analyses, p < 0.05 was considered statistically
significant and the SPSS software (v. 13.0) was used.
3. Results
Demographic characteristics and perioperative data are
shown in Table 1. No significant difference was obser-
ved between groups, with the exception of the number of
patients who received intraoperative adrenaline. Only
one patient in the Control Group who underwent neph-
rectomy needed pRBC intraoperatively after a hematocrit
value of 22% was detected.
In the intraoperative period, mean ± SD values of uri-
nary output in the Dexmedetomidine Group were sig-
nificantly higher than in the Control Group: 566 ± 396
mL and 298 ± 153 mL, respectively (p = 0.014). Cumu-
lative urinary output in 4, 12 and 24 hours after surgery
showed no difference between Dexmedetomidine Group
and Control Group, as follows, respectively: 837 ± 268
mL and 674 ± 197 mL (p = 0.30); 1230 ± 229 mL and
1077 ± 200 mL (p = 0.907); 1947 ± 266 mL and 1748 ±

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 358
237 mL (p = 0.91).
No significant changes were seen in postoperative
mean values of serum creatinine and creatinine clearance
for both, Dexmedetomidine Group and Control Group,
according to their baseline values. No significant differ-
ences between groups were detected at any time point for
these two variables (Table 2). Postoperative mean values
of serum cystatin C did not show any significant differ-
ence between groups at any moment and remained at the
normal range in both groups (Table 2).
The mean arterial pressure was significantly higher in
Dexmedetomidine Group before and after surgical inci-
sion (p < 0.05). Heart rate was significantly lower in the
Dexmedetomidine Group, both in the operating room and
Table 1. Characteristics and perioperative data of patients submitted to nephrectomy or prostatectomy receiving intraopera-
tive dexmedetomidine (Dexmedetomidine Group) or 0.9% saline (Control Group).
Dexmedetomidine Group (n = 15)Control Group (n = 15) p value
Age (years) 51 ± 13 56 ± 10 0.284
Weight (kg) 72 ± 11 68 ± 9 0.200
Height (cm) 167 ± 7 168 ± 6 0.574
Sex (Male/Female) 11/4 10/5 0.690
ASA (I/II) 5/10 9/6 0.143
Surgery (nephrectomy/prostatectomy) 9/6 6/9 0.308
Length of surgery (minutes) 227 ± 101 230 ± 70 0.852
Total volume of lactated Ringer’s (mL) 1900 + 920 2053 + 924 0.546
Total volume of HES (mL) 900 + 660 813 + 360 0.858
Use of adrenaline in the operating room (n) 5 11 0.028
Use of adrenaline in the PACU (n) 2 0 0.143
Age, weight, height and length of surgery, total volume of lactated Ringer’s and hydroxyethyl starch (HES) are expressed as mean ± SD. American Society of
Anesthesiologists (ASA) physical status, type of surgery, use of adrenaline in the operating room and in post anesthesia care unit (PACU) are expressed as
number of patients. No significant differences were seen between groups, excepted on the use of adrenaline in the operating room.
Table 2. Mean values and standard deviation for baseline and postoperative serum creatinine and calculated creatinine
clearance, and postoperative serum cystatin C of patients submitted to nephrectomy or prostatectomy receiving intraopera-
tive dexmedetomidine or 0.9% saline (Control). No significant differences were noted between groups.
1 Day 2 Days 3 Days 2 Weeks
Baseline
After surgery
p value (ANOVA)
Serum creatinine (mg/dL)
Dexmedetomidine 0.90 ± 0.16 1.09 ± 0.25 1.06 ± 0.28 1.00 ± 0.28 1.00 ± 0.19 0.260
Control 0.89 ± 0.18 0.95 ± 0.19 0.94 ± 0.25 0.89 ± 0.19 0.88 ± 0.16 0.773
p value 0.881 0.093 0.126 0.290 0.088
Creatinine clearance (mL/min)
Dexmedetomidine 97.9 ± 24.5 82.6 ± 26.5 86.4 ± 30.7 91.3 ± 30.0 88.1 ± 23.1 0.454
Control 88.9 ± 27.8 81.9 ± 22.6 85.5 ± 29.1 87.7 ± 23.4 87.9 ± 24.6 0.916
p value 0.358 0.785 0.731 0.919 0.947
Serum cystatin C (mg/L)
Dexmedetomidine 0.80 ± 0.37 0.90 ± 0.39 0.82 ± 0.33 0.85 ± 0.20 0.846
Control 0.75 ± 0.18 0.84 ± 0.19 0.84 ± 0.19 0.85 ± 0.14 0.217
p value 0.631 0.127 0.461 0.966

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 359
PACU (p < 0.05) (Figure 1).
4. Discussion
In this study, oncological patients were submitted to
prostatectomy or nephrectomy and, besides an intraop-
erative increase in diuresis, no effects on postoperative
renal function were observed with intraoperative infusion
of dexmedetomidine.
Patients with urogenital cancer may develop renal
dysfunction due to intrinsic renal disease or obstruction
in the urinary tract. For these patients, the risk of aggra-
vation in renal impairment is increased in the periopera-
tive period [12]. It is well established that preoperative
renal function, age, obesity, diabetes, hypertension and
proteinuria, as well as the type of surgery, are prognostic
factors for development of postoperative renal dysfunc-
tion [13]. The reduction in the glomerular filtration rate
is an independent risk factor for cardiovascular events
and mortality [14]. Therefore, strategies to preserve
postoperative renal function have been searched. These
strategies involve an adequate blood volume and perfu-
sion of the renal tissue, avoidance of nephrotoxins expo-
sure and some pharmacological methods with non-uni-
form efficacy [15].
Dexmedetomidine is an α2-agonist agent with an im-
portant sympatholytic activity [16] that reduces stress
response to surgical procedures [17] and in intensive care
units [18]. A possible beneficial effect on glomerular
filtration rate was shown in both animal [19] and human
studies [20]. Frumento et al. showed that dexmede-
tomidine improved renal performance after thoracotomy
[11].
Incidence of AKI varies not only with the profile of
the population studied, but also with the criteria used for
evaluation, size and type of surgery. Sorbellini et al.
studying patients after nephrectomy, found 14% of AKI
[21]. A retrospective analysis of 225 patients who un-
derwent nephrectomy showed a total of 43% incidence of
AKI [13]. In the present study, according to the criteria
used to assess renal function, two weeks after surgery
renal function was similar to preoperative values in both
groups and no influence of dexmedetomidine could be
Figure 1. Mean values and SD for mean arterial pressure (bottom) and heart rate (top) at operating room and at post anes-
thesia care unit (PACU) of patients submitted to nephrectomy or prostatectomy receiving intraoperative dexmedetomidine
) or 0.9% saline (). *p < 0.05 vs. control group. (

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 360
determined. Probably, rigorous hemodynamic control
and overall anesthetic management had a more important
role in renal function than dexmedetomidine itself could
have.
The significant increase in the intraoperative urine
output with dexmedetomidine infusion confirms the find-
ings of other authors [11,22]. The drug induces diuresis
in animal models, possibly due to its sympatholytic
property on the renal nerve [23]. It was also shown that
dexmedetomidine decreases secretion and/or action of
vasopressin, although it is unclear whether the diuretic
effect is due in part to a better renal perfusion [16,19].
Dexmedetomidine increases secretion of the atrial natri-
uretic peptide which results in natriuresis [8] and inhibits
renin secretion by the kidney [9]. Some studies have
shown that not only diuresis but also perioperative renal
function may be improved by α2-agonists [24]. However,
others [7,9] as well as the present study failed to show
such benefit.
Cystatin C is an endogenous marker of renal function
since it is freely filtered at the glomeruli and almost
completely reabsorbed and catabolized in the proximal
tubular cells [1]. In some studies, performance of this
marker was considered superior to that of creatinine in
the early diagnosis of renal dysfunction [25]. However,
some other authors have not confirmed such superiority
[26]. Kleber et al. [27] observed that the glomerular fil-
tration rate estimated from serum creatinine was superior
to that estimated by cystatin C in determining the initial
stages of renal dysfunction. The study also points to a
possible influence of some oncological diseases on cys-
tatin C concentration. Although creatinine is specific,
albeit not very sensitive, its levels do not significantly
increase until the glomerular filtration rate falls to values
lower than 50% of normal levels. Creatinine concentra-
tion is influenced by several factors, resulting in a large
variation among individuals. Ahlstrom et al. prospec-
tively analyzed 202 patients admitted to the intensive
care unit, and concluded that creatinine was as efficient
as cystatin C in detecting AKI [28].
Activation of α2 receptors promotes a significant re-
duction in circulating catecholamines, with moderate
reduction in heart rate and blood pressure [16,22,29].
Regarding heart rate, our results followed those of these
studies. In contrast, as reported by Dyck et al. [30], a
significant increase in mean arterial pressure was ob-
served in relation to the Control Group. This fact may be
related to the different regimens of drug administration
and associated techniques [8,22,23].
The limitations of this study are that just one dose of
dexmedetomidine was analyzed and different doses
could have had a different response. Besides, evaluation
of renal function was done by the mean of all subjects, a
method similar to that seen in Frumento’s study [11].
This may be criticized as small variations in serum crea-
tinine values may result in the first stage of AKI [31].
Nonetheless, as we intended to study the overall profile,
mean values of creatinine seem to be suitable. Creatinine
is a common and cheap marker to analyze renal function.
We understand that other more sensitive markers could
also have a different behavior.
5. Conclusion
In conclusion, according to the doses used in this study,
despite an intraoperative increase in diuresis, intraopera-
tive infusion of dexmedetomidine did not influence renal
performance up to two weeks after major uro-oncologic
surgery as evaluated by serum creatinine, creatinine clea-
rance and serum cystatin C.
6. Acknowledgements
PNJ was supported by Fundação de Amparo à Pesquisa
do Estado de São Paulo (FAPESP), grant # 09/51984-5.
REFERENCES
[1] D. R. Jones and H. T. Lee, “Perioperative Renal Protec-
tion,” Best Practice & Research Clinical Anaesthesiology,
Vol. 22, No. 1, 2008, pp. 193-208.
http://dx.doi.org/10.1016/j.bpa.2007.08.005
[2] G. M. Chertow, E. Burdick, M. Honour, J. V. Bonventre
and D. W. Bates, “Acute Kidney Injury, Mortality, Leng-
th of Stay, and Costs in Hospitalized Patients,” Journal of
the American Society of Nephrology, Vol. 16, No. 11,
2005, pp. 3365-3370.
http://dx.doi.org/10.1681/ASN.2004090740
[3] R. N. Sladen, “Anesthetic Considerations for the Patient
with Renal Failure,” Anesthesiology Clinics of North
America, Vol. 18, No. 4, 2000, pp. 863-882.
http://dx.doi.org/10.1016/S0889-8537(05)70199-1
[4] A. Cho, J. E. Lee, G. Y. Kwon, W. Huh, H. M. Lee, Y. G.
Kim, D. J. Kim, H. Y. Oh and H. Y. Choi, “Post-Opera-
tive Acute Kidney Injury in Patients with Renal Cell Car-
cinoma Is a Potent Risk Factor for New-Onset Chronic
Kidney Disease after Radical Nephrectomy,” Nephrology
Dialysis Transplantation, Vol. 26, No. 11, 2011, pp.
3496-3501. http://dx.doi.org/10.1093/ndt/gfr094
[5] R. Venkataraman and J. A. Kellum, “Prevention of Acute
Renal Failure,” Chest, Vol. 131, No. 1, 2007, pp. 300-308.
http://dx.doi.org/10.1378/chest.06-1246
[6] J. E. Hall, T. D. Uhrich, J. A. Barney, S. R. Arain and T. J.
Ebert, “Sedative, Amnestic, and Analgesic Properties of
Small-Dose Dexmedetomidine Infusions,” Anesthesia &
Analgesia, Vol. 90, No. 3, 2000, pp. 699-705.
http://dx.doi.org/10.1097/00000539-200003000-00035
[7] K. Leino, M. Hynynen, J. Jalonen, M. Salmenpera, H.
Scheinin and R. Aantaa, “Renal Effects of Dexmedeto-
midine during Coronary Artery Bypass Surgery: A Ran-
domized Placebo-Controlled Study,” BMC Anesthesiol-
ogy, Vol. 11, 2011, p. 9.

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 361
http://dx.doi.org/10.1186/1471-2253-11-9
[8] A. Bekker and M. K. Sturaitis, “Dexmedetomidine for
Neurological Surgery,” Neurosurgery, Vol. 57, No. 1,
2005, pp. 1-10.
http://dx.doi.org/10.1227/01.NEU.0000163476.42034.A1
[9] A. Bayram, A. Esmaoglu, A. Akin, G. Baskol, R. Aksu, C.
Bicer, A. Demirtas, R. Mutluay and A. Boyaci, “The Ef-
fects of Intraoperative Infusion of Dexmedetomidine on
Early Renal Function after Percutaneous Nephrolitho-
tomy,” Acta Anaesthesiologica Scandinavica, Vol. 55, No.
5, 2011, pp. 539-544.
http://dx.doi.org/10.1111/j.1399-6576.2011.02427.x
[10] D. W. Cockcroft and M. H. Gault, “Prediction of Crea-
tinine Clearance from Serum Creatinine,” Nephron, Vol.
16, No. 1, 1976, pp. 31-41.
http://dx.doi.org/10.1159/000180580
[11] R. J. Frumento, H. G. Logginidou, S. Wahlander, G. Wa-
gener, H. R. Playford and R. N. Sladen, “Dexmedetomi-
dine Infusion Is Associated with Enhanced Renal Func-
tion after Thoracic Surgery,” Journal of Clinical Anesthe-
sia, Vol. 18, No. 6, 2006, pp. 422-426.
http://dx.doi.org/10.1016/j.jclinane.2006.02.005
[12] P. Shenoy, P. Ward and T. Wigmore, “Surgical Manage-
ment of Urological Malignancy: Anaesthetic and Critical
Care Considerations,” Current Anaesthesia & Critical
Care, Vol. 20, No. 1, 2009, pp. 22-27.
http://dx.doi.org/10.1016/j.cacc.2008.10.005
[13] Y. Xu and B. Wu, “Prognostic Factors for Renal Dys-
function after Nephrectomy in Renal Cell Carcinomas,”
Journal of Surgical Research, Vol. 166, No. 1, 2011, pp.
e53-e57. http://dx.doi.org/10.1016/j.jclinane.2006.02.005
[14] A. S. Go, G. M. Chertow, D. Fan, C. E. McCulloch and C.
Y. Hsu, “Chronic Kidney Disease and the Risks of Death,
Cardiovascular Events, and Hospitalization,” The New
England Journal of Medicine, Vol. 351, No. 13, 2004, pp.
1296-1305. http://dx.doi.org/10.1056/NEJMoa041031
[15] S. A. Josephs and C. V. Thakar, “Perioperative Risk As-
sessment, Prevention, and Treatment of Acute Kidney
Injury,” International Anesthesiology Clinics, Vol. 47, No.
4, 2009, pp. 89-105.
http://dx.doi.org/10.1097/AIA.0b013e3181b47e98
[16] P. Talke, C. A. Richardson, M. Scheinin and D. M. Fisher,
“Postoperative Pharmacokinetics and Sympatholytic Ef-
fects of Dexmedetomidine,” Anesthesia & Analgesia, Vol.
85, No. 5, 1997, pp. 1136-1142.
[17] F. G. Curtis, Y. M. Castiglia, A. A. Stolf, E. Ronzella, S.
M. Vanni and P. Nascimento Junior, “Dexmedetomidine
and Sufentanil as Intraoperative Analgesics: Comparative
Study,” Revista Brasileira de Anestesiologia, Vol. 52, No.
5, 2002, pp. 525-534.
[18] R. M. Venn, C. J. Bradshaw, R. Spencer, D. Brealey, E.
Caudwell, C. Naughton, A. Vedio, M. Singer, R. Feneck,
D. Treacher, S. M. Willatts and R. M. Grounds, “Preli-
minary UK Experience of Dexmedetomidine, a Novel
Agent for Postoperative Sedation in the Intensive Care
Unit,” Anaesthesia, Vol. 54, No. 12, 1999, pp. 1136-1142.
http://dx.doi.org/10.1046/j.1365-2044.1999.01114.x
[19] N. R. Villela, P. do Nascimento Junior, L. R. de Carvalho
and A. Teixeira, “Effects of Dexmedetomidine on Renal
System and on Vasopressin Plasma Levels. Experimental
Study in Dogs,” Revista Brasileira de Anestesiologia, Vol.
55, No. 4, 2005, pp. 429-440.
[20] D. L. Herr, S. T. Sum-Ping and M. England, “ICU Seda-
tion after Coronary Artery Bypass Graft Surgery: Dex-
medetomidine-Based versus Propofol-Based Sedation
Regimens,” Journal of Cardiothoracic and Vascular An-
esthesia, Vol. 17, No. 5, 2003, pp. 576-584.
http://dx.doi.org/10.1016/S1053-0770(03)00200-3
[21] M. Sorbellini, M. W. Kattan, M. E. Snyder, A. A. Hakimi,
D. M. Sarasohn and P. Russo, “Prognostic Nomogram for
Renal Insufficiency after Radical or Partial Nephrecto-
my,” Journal of Urology, Vol. 176, No. 2, 2006, pp. 472-
476. http://dx.doi.org/10.1016/j.juro.2006.03.090
[22] A. M. De Wolf, R. J. Fragen, M. J. Avram, P. C. Fitzger-
ald and F. Rahimi-Danesh, “The Pharmacokinetics of
Dexmedetomidine in Volunteers with Severe Renal Im-
pairment,” Anesthesia & Analgesia, Vol. 93, No. 5, 2001,
pp. 1205-1209.
http://dx.doi.org/10.1097/00000539-200111000-00031
[23] H. Xu, M. Aibiki, K. Seki, S. Ogura and K. Ogli, “Effects
of Dexmedetomidine, an Alpha2-Adrenoceptor agonist,
on Renal Sympathetic Nerve Activity, Blood Pressure,
Heart Rate and Central Venous Pressure in Urethane-
Anesthetized Rabbits,” Journal of the Autonomic Nervous
System, Vol. 71, No. 1, 1998, pp. 48-54.
http://dx.doi.org/10.1016/S0165-1838(98)00061-7
[24] P. J. Kulka, M. Tryba and M. Zenz, “Preoperative Al-
pha2-Adrenergic Receptor Agonists Prevent the Deterio-
ration of Renal Function after Cardiac Surgery: Results of
a Randomized, Controlled Trial,” Critical Care Medicine,
Vol. 24, No. 6, 1996, pp. 947-952.
http://dx.doi.org/10.1097/00003246-199606000-00012
[25] V. R. Dharnidharka, C. Kwon and G. Stevens, “Serum
Cystatin C Is Superior to Serum Creatinine as a Marker of
Kidney Function: A Meta-Analysis,” American Journal
of Kidney Diseases, Vol. 40, No. 2, 2002, pp. 221-226.
http://dx.doi.org/10.1053/ajkd.2002.34487
[26] S. Herget-Rosenthal, S. Trabold, J. Huesing, U. Heemann,
T. Philipp and A. Kribben, “Cystatin C—An Accurate
Marker of Glomerular Filtration Rate after Renal Trans-
plantation?” Transplant International, Vol. 13, No. 4,
2000, pp. 285-289.
http://dx.doi.org/10.1111/j.1432-2277.2000.tb01083.x
[27] M. Kleber, M. Cybulla, K. Bauchmuller, G. Ihorst, B.
Koch and M. Engelhardt, “Monitoring of Renal Function
in Cancer Patients: An Ongoing Challenge for Clinical
Practice,” Annals of Oncology, Vol. 18, No. 5, 2007, pp.
950-958. http://dx.doi.org/10.1093/annonc/mdm055
[28] A. Ahlstrom, M. Tallgren, S. Peltonen and V. Pettila,
“Evolution and Predictive Power of Serum Cystatin C in
Acute Renal Failure,” Clinical Nephrology, Vol. 62, No.
5, 2004, pp. 344-350.
[29] K. Dere, I. Sucullu, E. T. Budak, S. Yeyen, A. I. Filiz, S.
Ozkan and G. Dagli, “A Comparison of Dexmedetomi-
dine versus Midazolam for Sedation, Pain and Hemody-
namic Control, during Colonoscopy under Conscious Se-
dation,” European Journal of Anaesthesiology, Vol. 27,

Renal Function after Major Uro-Oncologic Surgery and Dexmedetomidine Infusion 362
No. 7, 2010, pp. 648-652.
http://dx.doi.org/10.1097/EJA.0b013e3283347bfe
[30] J. B. Dyck, M. Maze, C. Haack, L. Vuorilehto and S. L.
Shafer, “The Pharmacokinetics and Hemodynamic Ef-
fects of Intravenous and Intramuscular Dexmedetomidine
Hydrochloride in Adult Human Volunteers,” Anesthesi-
ology, Vol. 78, No. 5, 1993, pp. 813-820.
http://dx.doi.org/10.1097/00000542-199305000-00002
[31] R. L. Mehta, J. A. Kellum, S. V. Shah, B. A. Molitoris, C.
Ronco, D. G. Warnock and A. Levin, “Acute Kidney In-
jury Network: Report of an Initiative to Improve Out-
comes in Acute Kidney Injury,” Critical Care, Vol. 11,
No. 2, 2007, p. R31. http://dx.doi.org/10.1186/cc5713