Diabetes Mellitus: a risk factor for drug toxicity

Author(s)

Chimirri de Limas Martins, Anna Luiza ^[1] ; Watanabe, Mirian ^{[1, 2]} ; Fernandes, Sheila Marques ^{[1, 3]} ; da Fonseca, Cassiane Dezoti ^{[1, 3]} ; Fernandes Vattimo, Maria de Fatima ^{[4, 1]}

Affiliation

^[1] Univ Sao Paulo, Lab Expt Modelos Anim, Escola Enfermagem, Sao Paulo, SP - Brazil

^[2] Univ Metropolitanas Unidas, Sao Paulo, SP - Brazil

^[3] Univ Sao Paulo, Programa Pos Grad Enfermagem Saude Adulto, Escola Enfermagem, Sao Paulo, SP - Brazil

^[4] Univ Sao Paulo, Dept Enfermagem Med Cirurg, Escola Enfermagem, Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: Revista da Escola de Enfermagem da USP; v. 52, 2018.
• Web of Science Citations: 0

Abstract

ABSTRACT Objective To assess the effect of the antibiotic Gentamicin in an experimental model in the presence of Diabetes Mellitus through renal function and oxidative profile. Method 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. Results 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. Conclusion The existence of Diabetes Mellitus resulted in an elevation of gentamicin nephrotoxicity, thus confirming the risk factor for drug nephrotoxicity. (AU)

• FAPESP's process: 11/24028-6 - EFFECT OF PHOSPHODIESTERASE-5 INIBITOR IN ISCHEMIC ACUTE KIDNEY INJURY IN RATS
• Grantee: Mirian Watanabe
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• FAPESP's process: 13/26560-2 - Iodinated contrast induced acute kidney injury in diabetic and nephropathy diabetic in rats
• Grantee: Maria de Fatima Fernandes Vattimo
• Support Opportunities: Regular Research Grants