Lesão renal aguda induzida pela sepse e potenciais terapias renoprotetoras

Abstract

Acute renal injury (AKI) is a common complication in critically ill patient and it is associated with high mortality, with sepsis being the most prevalent risk factor for renal failure in critically ill patients. LRA in sepsis is involved with oxidative stress and vasoconstriction. Therapeutic initiatives aimed at minimizing renal damage in sepsis were not confirmed. This study evaluated the systemic inflammatory response in sepsis, renal function and renoprotective effects of the vasodilator cilostazol and the antioxidants n-acetylcysteine (NAC) and diospenes hesperidin. Systemic parameters, the inflammatory renal, in the intestine and in the lungs profile (TGF-α and interleukin 6-IL-6), renal function (RF-creatinine clearance), urinary peroxides generation (PU) and histopathological analysis of the kidneys were performed. Male Wistar rats were divided into 5 groups: Sham (control); Sepsis: sepsis induced by the technique of ligation and puncture of the cecon (LPC); Sepsis+cilostazol; Sepsis+N-acetylcysteine (NAC) and Sepsis+diosmin. The results showed that the Sepsis group presented elevation of TGF-α and IL-6 and global parameters such as temperature reduction and hypotension characterizing the sepsis pattern. Sepsis groups showed reduced renal function and urinary flow and elevation on UPs. The Sepsis+Diosmina group was the only one to attenuate RF reduction and PU reduction when compared to the Sepsis group. All sepsis groups had renal histological changes. The study confirmed that sepsis induces AKI, being diosmin hesperidin the only agent to contribute to the improvement of renal function and reduction of oxidative stress.