Last update:
13-Nov-2007

This is a review of recent data concerning the pathogenesis and management of sepsis and of its common complication acute renal failure (ARF) in an effort to reduce the incidence of sepsis and ARF and improve therapeutic interventions. Host invasion by various infectious microorganisms or their toxic products causes activation of many defense mechanisms (cellular immunity, coagulation cascade, complement pathway, vascular endothelium and polymorphonuclear cells) and production of pro-inflammatory and inflammatory mediators, radical oxygen species and arachidonic acid derivatives, in order to minimize and eliminate the infectious threat. Activation of these defense mechanisms may in a variety of circumstances, become excessive and detrimental, resulting in uncontrolled systemic inflammatory reaction, defined as sepsis. The hallmark of sepsis is generalized arterial vasodilatation, which results in microcirculatory disturbances and inadequate tissue perfusion. Arterial underfilling due to arterial vasodilatation results in activation of the sympathetic nervous system and the reninangiotensin-aldosterone axis in the kidney, and finally renal vasoconstriction and ischemia. Many other factors such as cytokines, microvascular coagulation, immunological mechanisms, increased endothelin production, down-regulation of endothelial nitric oxide synthase (e-NOS) within the kidney and reduced production of nitric oxide (NO) all contribute to the occurrence of ARF in sepsis. ARF, manifested usually as acute tubular necrosis, but also as acute postinfectious glomerulonephritis, acute interstitial nephritis or acute cortical necrosis, is a common complication of sepsis affecting as many as 9-40% of septic patients. Development of ARF increases morbidity and mortality, and its management requires knowledge of the pathogenetic factors and of the complex therapeutic interventions available (conservative or the use of extracorporeal methods).