Abstract

To assess the effect of the antibiotic Gentamicin in an experimental model in the presence of Diabetes Mellitus through renal function and oxidative profile. Adult male Wistar rats were distributed into groups: Citrate; Gentamicin (Genta), (intraperitoneal, i.p. gentamicin, 100 mg/kg of body weight, once a day,5 days); DM (60 mg/kg of STZ (Streptozotocin), single dose, intravenously, i.v., diluted in citrate buffer); and DM+Genta. Physiological parameters, renal function (creatinine clearance), oxidative damage (peroxides and thiobarbituric acid reactive substances - urinary TBARS) and renal hemodynamics were evaluated. The Diabetes Mellitus group presented chronic hyperglycemia associated with loss of body weight, polyphagia, polydipsia and polyuria, in addition to reduced renal function and with an increase in oxidative metabolite excretion. Administration of gentamicin induced a reduction in renal blood flow and increased renal vascular resistance in healthy rats. The association of Diabetes Mellitus with gentamicin resulted in an additional reduction in renal function and elevation of oxidative metabolites, with increased renal vascular resistance. The existence of Diabetes Mellitus resulted in an elevation of gentamicin nephrotoxicity, thus confirming the risk factor for drug nephrotoxicity.

Highlights

  • Acute kidney injury (AKI) consists of an abrupt reduction of renal function (RF), clinically signaled by the elevation of serum creatinine to levels greater than or equal to 0.3 mg/dL in 48 hours, or a 1.5-fold increase in this marker over a 7-dayperiod[1]

  • AKI is less frequent in the general community than in hospitalized patients, and its prevalence is significant in Intensive Care Units (ICUs), affecting 20% to 40% of the patients hospitalized in these units[2]

  • It was possible to observe an increase in the weight of the citrate values for all groups (Citrate) group when compared

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Summary

Introduction

Acute kidney injury (AKI) consists of an abrupt reduction of renal function (RF), clinically signaled by the elevation of serum creatinine to levels greater than or equal to 0.3 mg/dL in 48 hours, or a 1.5-fold increase in this marker over a 7-dayperiod[1]. AKI is less frequent in the general community than in hospitalized patients, and its prevalence is significant in Intensive Care Units (ICUs), affecting 20% to 40% of the patients hospitalized in these units[2]. Gentamicin is an aminoglycoside antibiotic, widely used in the fight against gram-negative bacterial infections and has nephrotoxicity as one of its main side effects. This is because its excretion predominantly occurs by glomerular filtration. The pathophysiology of gentamicin nephrotoxicity is characterized by damage to tubular and glomerular renal cells[3,4],associated with oxidative stress, generation of reactive oxygen species (ROS) and reduced antioxidant enzymes in the kidney[5]

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