Abstract
To evaluate the preventive effect of ascorbic acid on sevoflurane-induced acute renal failure in an experimental rat model. Twenty-four adult male Wistar rats were randomly distributed into three groups. Subjects were allocated into 3 groups: Group I received sevoflurane only, whereas Groups II and III had moderate (150 mg/kg) and high (300 mg/kg) doses of AA in addition to sevoflurane, respectively. Rhabdomyolysis and myohemoglobinuric ARF was formed by intramuscular administration of glycerol on the upper hind limb on the 15th minute of inhalation anesthesia. Biochemical parameters consisted of serum levels of blood urea nitrogen, creatinine, neutrophil gelatinase-associated lipocalin (NGAL), total antioxidant capacity (TAC), and protein carbonyl content. Histopathological variables were tubular necrosis, fibrin, and cast formation. NGAL levels were significantly lower in Group III than Group II and Group I. On the other hand, TAC, PCO, urea and creatinine levels were notably higher in Group I compared with Groups II and III. There was a significant difference between 3 groups on frequencies of acute tubular necrosis (p=0.003), fibrin (p<0.001) and cast (p<0.001). Acute tubular necrosis and fibrin formation were more prominent in Group I. Casts were more common in Groups II and III. The ascorbic acid serve as a prophylactic agent against renal damage in patients receiving sevoflurane anesthesia and higher doses were associated with more apparent protective effects.
Highlights
Acute renal failure (ARF) may occur in the early postoperative period, and its incidence has been reported as 0.1%-30% after various surgical procedures[1,2]
Even though high doses of inorganic fluoride may lead to proximal tubular necrosis, it may have cytoprotective effect in low doses[5]
We comparatively evaluated the histopathological and biochemical outcomes of sevoflurane anesthesia on kidneys with and without Ascorbic acid (AA) in an acute tubular necrosis model triggered with glycerol
Summary
Acute renal failure (ARF) may occur in the early postoperative period, and its incidence has been reported as 0.1%-30% after various surgical procedures[1,2]. Postoperative ARF has been linked with many factors including perioperative hypotension and nephrotoxin-induced acute tubular necrosis. Type of anesthesia may significantly affect the likelihood of acute renal tubular damage[1]. Volatile anesthetics such as sevoflurane are commonly used in clinical practice, and they have different degrees and sites of metabolism[3]. Metabolic reactions during elimination of volatile anaesthetics may lead to elevation of nephrotoxic inorganic fluoride levels[4]. Even though high doses of inorganic fluoride may lead to proximal tubular necrosis, it may have cytoprotective effect in low doses[5]. Intramuscular glycerol injection causes a nephrotoxic (myohemoglobinuric)/ ATP depletion leading to acute tubular necrosis[6]
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