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Abstract Sepsis is a life-threatening condition that arises when the body’s response to infection injures its own tissues and organs. Sepsis is caused by an immune response triggered by an infection. The clinical diagnosis of sepsis requires finding a focus of infection as well as at least two signs of systemic inflammatory-response syndrome that comprise abnormal body temperature (higher than 38°C or less than 36°C), heart rate >90 beats/min, respiration >20 breaths/min or arterial partial pressure of CO2 <32 mmHg, and deranged white blood cell counts (greater than 12 x 103/mm3, less than 4 x 103/mm3, or greater than 10% bands). Sepsis has severe consequences, including multiple organ failure. It is well established that the kidney is a commonly affected organ during sepsis, and its involvement carries a high risk of mortality. Acute renal failure, is a rapidly progressive loss of renal function, generally characterized by oliguria (decreased urine production, quantified as less than 400 mL per day in adults and fluid and electrolyte imbalance. It is characterized by the sudden loss of the kidney capacity to excrete waste products, concentrate urine, preserve electrolytes and keep the water balance. It is particularly common in the intensive care unit (ICU), where it is associated to 50-80% mortality. Historically, acute renal failure during sepsis has been considered to be a consequence of diminished renal blood flow. Indeed, in early stages of sepsis or in sepsis associated to cardiogenic shock, RBF may decrease. Despite several advances in treatment and in understanding of the pathogenesis of ARF, many aspects in this field remain subject to controversy. |