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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 7  |  Issue : 3  |  Page : 282-290

Renal protective effects of dexmedetomidine in patients undergoing radical nephrectomy


Department of Anesthesia and Surgical Intensive Care, Faculty of Medicine, University of Alexandria, Alexandria, Egypt

Date of Submission29-Jun-2016
Date of Acceptance05-Aug-2018
Date of Web Publication29-Sep-2020

Correspondence Address:
Rania AA Sabra
Department of Anesthesia and Surgical Intensive Care, Faculty of Medicine, University of Alexandria, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/roaic.roaic_57_16

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  Abstract 

Background Acute kidney injury (AKI) after radical nephrectomy is a serious complication that increases morbidity and mortality rates. Early detection and prevention of this complication are very important. A novel biomarker named neutrophil gelatinase-associated lipocalin (NGAL) can play an important role in early diagnosis of AKI. Recent studies have been published on the favorable effects of dexmedetomidine on renal functions.
Objective The aim was to evaluate the possible renal protective effects of dexmedetomidine regarding urine output, creatinine clearance, serum cystatine C, NGAL in patients undergoing radical nephrectomy.
Patients and methods A randomized double-blind, placebo-controlled study was conducted on 30 adult patients scheduled for radical nephrectomy. The patients were randomly allocated into two equal groups. Dexmedetomidine group (D group) received dexmedetomidine 0.8 µg/kg intravenously over 10 min as a loading dose, and then it was infused at a rate of 0.4 µg/kg/h. Placebo group (P group) received normal saline instead of dexmedetomidine in the same volume (ml) and rate (ml/h). In both groups, fentanyl (0.5 µg/kg) boluses were given if blood pressure or heart rate (HR) showed 20% increase from the baseline reading to control the hemodynamics. Vital signs [HR and mean arterial blood pressure (MABP)] were recorded before induction, after induction, after intubation, intraoperatively every 10 min till the end of surgery, and postoperatively every 2 h during the first 24 h. Urine output was assessed intraoperatively every 1 h and postoperatively every 4 h in the first 48 h. Serum creatinine, urinary creatinine, and creatinine clearance were assessed 24 h before surgery, 24 h after urinary catheter insertion after induction of anesthesia, and 24–48 h postoperatively. Cystatine C and NGAL were assessed after induction of anesthesia and after 24 h and 48 h postoperatively. Sedation was assessed during the first 5, 15, 30, and 60 min in the recovery room by the investigator using a five-point sedation scale. Postoperative pain was assessed using the visual analog scale, based on 0–10 points, every hour in the first 4 h postoperatively and then every 4 h in the first postoperative day.
Results There was a significant decrease in HR and MABP in the dexmedetomidine group compared with placebo group. Urine output showed significant difference between the two groups in all studied periods except for the first hour. Urine output was higher in dexmedetomidine group, and seven patients in the placebo group needed lasix. Serum creatinine values, creatinine clearance, and cystatine C showed no statistically significant difference between the two groups in the three studied periods. NGAL values were similar after induction but were significantly different between the two groups after 24 and 48 h, with values higher in the placebo group. Sedation was different between the two groups in all studied periods except after 5 min. Patients in dexmedetomidine group were more sedated compared with the placebo group. Dexmedetomidine had postoperative analgesic effect represented by low visual analog scale score.
Conclusion Dexmedetomidine proved to be effective in the prophylaxis of postoperative AKI after radical nephrectomy in terms of NGAL values but did not affect renal functions in terms of serum creatinine, creatinine clearance, and cystatine C. Dexmedetomidine in the used dose did not have adverse effects on MABP and HR. In addition to renal protection, dexmedetomidine proved to have sedative and analgesic properties.

Keywords: dexmedetomidine, neutrophil gelatinase-associated lipocalin and cystatine C, postoperative acute kidney injury, radical nephrectomy


How to cite this article:
Sabra RA, Abdelhady MM, Afify MK, Omar SY. Renal protective effects of dexmedetomidine in patients undergoing radical nephrectomy. Res Opin Anesth Intensive Care 2020;7:282-90

How to cite this URL:
Sabra RA, Abdelhady MM, Afify MK, Omar SY. Renal protective effects of dexmedetomidine in patients undergoing radical nephrectomy. Res Opin Anesth Intensive Care [serial online] 2020 [cited 2020 Oct 23];7:282-90. Available from: http://www.roaic.eg.net/text.asp?2020/7/3/282/296618


  Introduction Top


Renal cell carcinomas (RCCs) are responsible for 80–85% of all primary renal neoplasms [1]. Because RCC is resistant to nonsurgical treatments (chemotherapy, hormonal therapy, and radiation), radical nephrectomy remains the reference standard of treatment. Surgical removal of the cancer is the most effective form of treatment for patients whose cancer is confined to the kidney [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 acute kidney injury (AKI). Postoperative AKI in patients with RCC is a potent risk factor for new-onset chronic kidney disease (CKD) after radical nephrectomy. Prevention of postoperative AKI is essential to limit the incidence of CKD after nephrectomy [4].

The diagnosis of AKI is usually based on measurements of blood urea nitrogen and serum creatinine. Blood urea nitrogen and serum creatinine are not very sensitive or specific for the diagnosis of AKI, because they are affected by many renal and nonrenal factors that are independent of kidney injury or kidney function [5].

Cystatine C is an endogenous marker of renal function, as it is freely filtered at the glomeruli and almost completely reabsorbed and catabolized in the proximal tubular cells [6]. In some studies, performance of this marker was considered superior to that of creatinine in the early diagnosis of renal dysfunction [7]. However, some other authors have not confirmed such superiority [8].

Serum neutrophil gelatinase-associated lipocalin (NGAL) is a highly sensitive, specific, and predictive early biomarker for AKI in a wide range of different disease processes. NGAL is a measure of tubular stress; its concentration increases dramatically in response to tubular injury and precedes increased in serum creatinine by more than 24 h [9].

Dexmedetomidine is a potent and more selective α2-adrenoreceptor agonist than clonidine. Compared with clonidine, dexmedetomidine has an α2 : α1-adrenoreceptor ratio of ∼1600 : 1 [10]. Dexmedetomidine is a potent and highly selective α2-adrenoceptor agonist with sympatholytic, sedative, amnestic, and analgesic properties [11],[12] and has been described as a useful and safe adjunct in many clinical applications.

This study was done to evaluate possible renal protective effects of dexmedetomidine regarding urine output, creatinine clearance, serum cystatine C, and NGAL in patients undergoing radical nephrectomy.


  Patients and methods Top


After obtaining a written informed consent from each patient, randomized, double-blind and placebo-controlled study was done, which included 30 adult patients scheduled for radical nephrectomy. After approval of the ethical committee and obtaining a written informed consent from each patient. Patients with history of use of α2-agonists to treat hypertension, previous treatment with dexmedetomidine, renal impairment (creatinine clearance less than 90 ml/min), and persistent intraoperative hypotension [mean arterial blood pressure (MABP) <65 for >20 min] were excluded from the study.

Patients were randomly allocated into equal two groups of 15 patients each: dexmedetomidine (D) group, where dexmedetomidine (0.8 µg/kg) was given intravenously over 10 min as a loading dose, and then infused at a rate of 0.4 µg/kg/h; and placebo group (P group), where normal saline instead of dexmedetomidine was given in volume (ml) and rate (ml/h) calculated according to the body weight. The infusion was started after induction of anesthesia and continued 24 h postoperatively.

In all patients, anesthesia was induced with fentanyl (1.5–2 µg/kg), lidocaine (100 mg), and propofol (1–2 mg/kg). For facilitating endotracheal intubation, atracurium was administered at an initial dose of 0.5 mg/kg followed by boluses of 0.03 mg/kg every 20–40 min.

Under aseptic technique, an arterial line and central venous catheter were inserted following induction of anesthesia.

Anesthesia was maintained using isofurane 1–2% in oxygen, and patients were mechanically ventilated. Fentanyl and atracurium increments were given as required. In both groups, fentanyl (0.5 µg/kg) boluses were given if blood pressure or heart rate (HR) showed 20% increase from the baseline reading to control the hemodynamics. Intraoperative hypotension was treated with an increase in intravascular volume and if persisted more than two readings, patients were given 5 mg ephedrine which could be repeated 3 times and patients who received ephedrine were excluded from the study. Fluids were given based on an estimation of the following:
  1. Fluid losses before the start of anesthesia.
  2. Maintenance requirements.
  3. Normal fluid losses that occur during surgery.
  4. Response to unanticipated fluid (blood) loss. Urine output was assessed hourly during intraoperative period and then every 4 h postoperatively for 48 h.


Oliguria is defined as urine output less than 0.5 ml/kg/h. After exclusion of catheter obstruction, patients with oliguria were managed with good hydration. If it persists, a trial of intravenous furosemide was attempted, starting with 20-mg lasix that could be repeated twice. If oliguria persists, nephrology consultation was required for further evaluation.

By the end of surgery, anesthestics were stopped. Muscle relaxants were antagonized by neostigmine 0.04–0.06 mg/kg and atropine 0.02 mg/kg, and then the patient was extubated after returning to full muscle power. All patients were monitored in the intensive care unit after operation for 2 days, with attention to fluid balance and urine output. All patients received 50-mg pethidine intramuscularly as a preventive analgesia immediately postoperatively.

Postoperative pain was assessed using the visual analog scale from 0–10. If the scale is 4 or more, a rescue dose of 10-mg pethidine was given and repeated every 10 min till the scale is less than 4.

Data management

Data were fed to the computer and analyzed using IBM SPSS software package version 20.0 (Armonk, NY: IBM Corp). Quantitative data were described using range (minimum and maximum), mean, SD, and median. Significance of the obtained results was judged at the 5% level.


  Results Top


The preoperative baseline MABP and HR values were similar in the two groups ([Table 1] and [Table 2]).
Table 1 Comparison between the two studied groups according to heart rate in intraoperative period

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Table 2 Comparison between the two studied groups according to mean arterial blood pressure in intraoperative period

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There was no statistically significant difference between the two groups regarding HR and MABP in the following periods: before induction, after induction, after intubation, and first reading in the first hour; thereafter, HR and MABP significantly decreased in the remaining periods ([Table 1] and [Table 2], [Figure 1] and [Figure 2]). It was observed that there was no bradycardia or hypertension in dexmedetomidine group ([Figure 3]).
Figure 1 Comparison between the two studied groups according to VAS.

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Figure 2 Comparison between the two studied groups according to heart rate in postoperative period.

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Figure 3 Comparison between the two groups as regards Change in MABP in postoperative period.

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Urine output was higher in dexmedetomidine group, and seven patients in placebo group needed lasix ([Figure 4]).
Figure 4 Comparison between the two studied groups according to urinary output.

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Serum creatinine, creatinine clearance, and cystatin C values were similar in the two groups in the three studied periods ([Table 3] and [Table 4]).
Table 3 Comparison between the two studied groups according to serum creatinine and creatinine clearance

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Table 4 Comparison between the two studied groups according to cystatine C and neutrophil gelatinase-associated lipocalin values

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NGAL values were similar after induction but were higher in placebo group after 24 and 48 h.

Sedation score was similar after 5 min, but patients in dexmedetomidine group were more sedated in the remaining periods ([Table 5]).
Table 5 Comparison between the two studied groups according to sedation score

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Postoperative visual analogue scale showed lower pain scores in dexemetomidine group in all measured times.


  Discussion Top


The hemodynamic effects of dexmedetomidine in the present study showed lower MABP and slower HR starting after 10 min of intraoperative hour and continued in both the intraoperative and postoperative periods.

These results were in agreement with the results of Tanskanen et al. [13] who found that intraoperative infusion of dexmedetomidine at a rate of 0.4 µg/kg/h maintains HR and blood pressure in acceptable range for a longer duration as compared with placebo group. The decrease in HR and blood pressure is similar to the findings by Feld et al. [14], who compared dexmedetomidine with fentanyl in bariatric surgery, thus showing that dexmedetomidine by its sympatholytic activity attenuates various stress responses during surgery and maintains hemodynamic stability. Jagadish et al. [15] showed that dexmedetomidine infusion 1 µg/kg before induction of anesthesia and then continuous infusion at a dose of 0.2–0.7 µg/kg/h intraoperatively caused decrease in arterial blood pressure and HR with maintenance of hemodynamic stability in patients scheduled for elective surgeries (e.g. thyroidectomy and abdominal surgeries) under general anesthesia.

In the present study, no patient had bradycardia in dexmedetomidine group, which was in agreement with the study by Gurbet et al. [16], who reported that bradycardia did not develop in patients scheduled for total abdominal hysterectomy and received a loading dose of dexmedetomidine 1 µg/kg intravenously during induction of anesthesia, followed by a continuous infusion at a rate of 0.5 µg/kg/h. On the contrary, Keniya et al. [17] in their study assessing the efficacy of dexmedetomidine in attenuating sympathoadrenal response to tracheal intubation and analyzing reduction in intraoperative anesthetic requirement found that two patients who received dexmedetomidine had bradycardia without decrease in arterial blood pressure and responded to intravenous atropine.

Dexmedetomidine can cause an increase in blood pressure and a decrease in HR with large concentrations or with rapid infusion rates [18],[19],[20]. Activation of α2-adrenoceptors on vascular smooth muscle is thought to result in vasoconstriction, increased blood pressure, and probable reflex decreased HR [18],[19],[20]. In the present study, there was neither decrease of HR nor increase of blood pressure during the bolus infusion. This suggests that initial 1 µg/kg loading infusion for 10 min is not rapid and may not cause large blood concentrations of dexmedetomidine.

In the present study, there were no statistically significant differences between the two groups regarding serum creatinine, creatinine clearance, and cystatine C. Moreover, there was no statistically significant difference between the two groups regarding urinary creatinine in the preoperative value and after 24 h, but it was significant after 48 h.

The present study demonstrated statistically significant difference between the two groups regarding urinary output in all studied periods, except for the first hour, where urine output was higher in dexmedetomidine group. Six patients received lasix in the placebo group.

In agreement with our results was the study conducted by Novaes et al. [21] on patients scheduled for nephrectomy or prostatectomy. Patients were divided into two groups for blind infusion of dexmedetomidine 0.5 µg/kg in the first 20 min followed by an infusion of 0.7 µg/kg/h until the end of surgery or 0.9% saline. No significant changes were seen in postoperative mean values of serum creatinine and creatinine clearance for both dexmedetomidine group and control group. Postoperative mean values of serum cystatine C did not show any significant difference between groups at any moment and remained at the normal range in both groups.

Moreover, Leino et al. [22] in a study evaluated the renal effects of dexmedetomidine during coronary artery bypass surgery, and dexmedetomidine infusion was started immediately after anesthesia induction and continued until 4 h after arrival in the ICU. Dexmedetomidine did not alter renal function, although it was associated with an increase in urinary output as compared with placebo. In line with our results, Salah et al. [23] in a study carried out on patients with mild to moderate renal impairment and scheduled for elective CABG showed dexmedetomidine infusion was started after induction of anesthesia and continued until the end of surgery. In this study, dexmedetomidine infusion did not alter renal function in terms of serum creatinine or creatinine clearance but was associated with an increase in urinary output in the first 24 h.

In the present study, there was a statistically significant difference between the two groups regarding serum NGAL values after 24 and 48 h. Conventional renal function tests, including blood urea nitrogen, serum creatinine, urine output, and creatinine clearance rate measurements, typically may not detect the development of acute kidney dysfunction in the first 48-h postoperative period. Differences detected in the renal function in the early postoperative period as determined by measurements of blood NGAL levels were significant.

In agreement with our results was the study conducted by Balkanay et al. [24], on 90 patients scheduled for CABG. The patients were divided into three groups: the first group received a placebo, and the second and the third groups received 4 and 8 µg/ml concentrations of the dexmedetomidine infusion, respectively. Results of conventional renal function tests were not significantly different. However, NGAL levels for the first postoperative day for placebo and low-dose and high-dose dexmedetomidine groups were significantly different among the groups. In line with our results was the study carried out by Suriyachote et al. [25], on patients undergoing CABG surgery with normal renal function. Dexmedetomidine was given at a bolus of 0.5 µg/kg in 20 min and infused at 0.4 µg/kg/h until the end of the operation. Plasma NGAL in dexmedetomidine group was significantly less than control group at 6 and 24 h. Serum creatinine was not significantly different between groups. Moreover, dexmedetomidine group had significantly higher urine output throughout the operation, confirming that dexmedetomidine reduced AKI in elective CABG patients when using NGAL as a biomarker.

In support of our results, Bayram et al. [26] investigated the effects of dexmedetomidine on early-stage renal function in pediatric patients undergoing cardiac angiography. In this study, contrast-induced AKI developed in 10% of the patients in dexmedetomidine group and 36.7% of the patients in placebo group, and NGAL values were significantly increased in patients with CIN in both groups. In contrast to our results, Bayram et al. [27] evaluated the effects of intraoperative infusion of dexmedetomidine on early renal function after percutaneous nephrolithotomy and found that intraoperative infusion of dexmedetomidine was not found to have beneficial effects on creatinine clearance, NGAL, or cystatine C levels early after the procedure; however, it reduced renin levels. The contrast may be because of the different type of surgery or limited duration of dexmedetomidine infusion (intraoperative only).

Effects of dexmedetomidine on renal functions have recently been intensively investigated among both animals and humans. In an experimental study in dogs, Villela et al. [28] evaluated the effects of dexmedetomidine on renal system and on vasopressin plasma levels and founded that low doses of dexmedetomidine inhibit vasopressin secretion, causing aqueous dieresis, and these actions might protect kidneys during ischemic events. Another experimental study [29] demonstrated that before or after treatment with dexmedetomidine provided cytoprotection and improved tubular architecture and function following renal ischemia. Consistent with this cytoprotection, dexmedetomidine reduced plasma high-mobility group protein B1 elevation when given before or after kidney ischemia–reperfusion; pretreatment also decreased toll-like receptor 4 expression in tubular cells. Dexmedetomidine treatment provided long-term functional renoprotection, and even increased survival following nephrectomy.

In evaluating the renoprotective effects of α2-agonists, Myles et al. [30] in a study carried out on patients undergoing elective CABG surgery showed that patients who received clonidine were associated with a significant higher creatinine clearance, and they attributed that the renal protective effects of clonidine occur by means of attenuating the sympathetic activation.

Moreover, Kulka et al. [31] in their study on patients undergoing CABG surgery concluded that preoperative treatment with clonidine (4 µg/kg) prevents the deterioration of renal function after cardiac surgery.

Confirming the renoprotective effects of dexmedetomidine, Ji et al. [32] in a retrospective study involving 1219 consecutive cardiac surgeries demonstrated that postbypass dexmedetomidine use is associated with a significant reduction in the incidence of AKI, especially mild AKI, in patients with preoperative normal renal function and mild CKD undergoing cardiac surgery. The postbypass use of dexmedetomidine is also associated with a significant decrease in in-hospital, 30-day mortality and the incidence of postoperative overall complications.

In support of the present study was the study carried out by Cho et al. [33] on patients scheduled for cardiac surgery, where dexmedetomidine was continuously infused at a rate of 0.4 mg/kg/h starting immediately after anesthetic induction and continued for 24 h after the surgery. They found that the incidence of AKI was significantly lower in the dexmedetomidine group (14%) than in the control group (33%). Moreover, the severity of AKI in the dexmedetomidine group was confined to stage 1 according to AKIN criteria except in one patient, whereas more severe stages of injury (stage 2 or 3) were observed in 14 patients in the control group, including five patients who required renal replacement therapy.

In contrast to the results of Cho et al. [33], a study carried out by Ji et al. [34] on patients who underwent cardiac surgery, the use of dexmedetomidine was associated with an increase in the incidence of postoperative renal dysfunction. The contrary results in this study might reflect the timing of dexmedetomidine administration, because the beneficial effect may require the administration of the drug before the renal insult. In addition, in this study, the incidence of preoperative renal failure was greater in the dexmedetomidine group.

One recent study examined the underlying mechanisms of positive effects of dexmedetomidine on renoprotection against ischemia and reperfusion injury [35]. They showed that dexmedetomidine protects the kidney against ischemia and reperfusion injury. The underlying mechanism was thought to be dexmedetomidine’s inhibitory effect on injury-induced activation of the Janus kinase/signal transducers and activators of transcription signaling pathway. Their suggestions for the use of dexmedetomidine also reflect our approach to our study and support our results.

Regarding the postoperative sedation score, in the present study, there was a statistically significant difference between the two groups regarding sedation in all studied periods except after 5 min. Patients showed a significant increase in sedation score after 5 min in dexmedetomidine group. This was attributed to the fact that dexmedetomidine has sedative properties. In agreement with our results, Manasa et al. [36] studied the effects of single intravenous dose of dexmedetomidine in postoperative period, where patients received 1 µg/kg of dexmedetomidine intravenously over 20 min. They found that single intravenous dose of dexmedetomidine could provide adequate sedative, analgesic, and anxiolytic effects with no accompanying respiratory depression, thereby minimizing polypharmacy.

Regarding postoperative pain score, the present study showed statistically significant difference between the two groups in all periods except in the seventh and 19th hour. Pain score values were lower in dexmedetomidine group. This was attributed to the analgesic effects of the drug.

In agreement with our results, Jaakola et al. [37] evaluated analgesia after systemic administration of different doses of dexmedetomidine (0.25, 0.50, and 1 µg/kg) and fentanyl (2 µg/kg) in healthy volunteers and found that dexmedetomidine had a moderate analgesic effect that was maximized at 0.5 µg/kg.

Moreover, Kumar et al. [38] carried out a study to compare the effects of dexmedetomidine and clonidine premedication in perioperative hemodynamic stability and postoperative analgesia in laparoscopic cholecystectomy. In this study, dexmedetomidine provided reliable postoperative analgesia.

In conclusion, dexmedetomidine proved to be effective in the prophylaxis of postoperative AKI after radical nephrectomy in terms of NGAL and preservation of urine output but did not affect renal functions in terms of serum creatinine, creatinine clearance, and cystatine C.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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