Renal effects of dexmedetomidine as an adjunct to general anesthesia combined with epidural anesthesia in patients undergoing Uro-Oncologic Surgery

INTRODUCTION: Acute kidney injury (AKI) in the perioperative period is associated with increased morbidity and postoperative mortality. Among the pharmacologic strategies for preventing agents are α-2 agonists. This study aimed to evaluate the role of dexmedetomidine on renal function after major uro-oncologic surgery, with serum cystatin C, serum creatinine and serum vasopressin. METHODS: Thirty cancer patients with serum creatinine < 1.3 mg/kg scheduled for prostatectomy or nephrectomy were anesthetized with epidural ropivacaine 0.75%, 20 ml, followed by general anesthesia with target controlled infusion of propofol, 0,2 mg/kg cisatracurium and 1.5 mg/kg lidocaine before tracheal intubation. They were randomly assigned to either blinded infusion of dexmedetomidine (Dexmedetomidine group, n = 15, 1 µg/kg/h for 20 minutes, followed by 0.7 µg/kg/h throughout the surgery), or saline (Control group, n = 15, 0.9% NaCl, same infusion rate protocol). The renal parameters were perioperative urinary output (UO) and the daily levels of plasma creatinine and cystatin C for 3 days and after 2 to 4 weeks postoperatively. Patients were classified according to the AKI criteria. RESULTS: Groups were homogeneous according to demographic variables, length of surgery and infusion of fluids (p > 0.05). Heart rate was lower in the Dexmedetomidine group during surgery and in the postanesthesia care unit (p < 0.05). Mean arterial pressure was higher in the Dexmedetomidine group (p < 0.05) during surgery. The intraoperative UO was higher in the Dexmedetomidine group (mean ± SD: DEX, 566 ± 396 ml; Control, 298 ± 153 ml, p < 0.05) but no differences were observed in the cumulative diuresis 24 hours after surgery (mean ± SD: Dexmedetomidine, 1947 ± 266 ml; Control, 1748 ± 237 ml, p > 0.05). Postoperatively four patients in the Dexmedetomidine group and 3 patients in the Control group (p > 0.05) were classified as with stage-1 AKI (serum creatinine increase > 0.3 = mg/kg or an increase of 1.5 to 2-fold from baseline serum creatinine). Two patients in the Dexmedetomidine group but none in the Control group (p > 0.05) were classified as with stage-2 AKI (serum creatinine increase = 2 to 3-fold from baseline serum creatinine). Two patients with stage-1 AKI from each group did not recovered renal function and one patient in the Dexmedetomidine group was reclassified from stage-2 to stage-1 AKI at the 2-4 week follow-up. At all times, the mean values of cystatin C were within the normal range in both groups, without differences between groups (p > 0.05). Values for cystatin C were normal in the Control group in all patients and four patients in the Dexmedetomidine group with AKI, had cystatin C above normal values. The plasma vasopressin showed large variations in both groups and at all times, with no significant difference between groups (p > 0.05). All patients with postoperative AKI underwent nephrectomy exhibiting significant difference in comparison with those who underwent prostatecomy (p < 0.01). CONCLUSION: Dexmedetomidine does not prevent the AKI in major Uro-Oncologic Surgery.