title: [Physiopathology of acute renal failure during sepsis].
abstract: Acute renal failure (ARF) is an independent risk factor associated with increased mortality during sepsis. Recent consensus definitions have allowed the standardization of research on the subject. The understanding of the physiopathology of ARF during sepsis is limited by the scarcity of histological studies and the inability to measure renal microcirculatory flows. Historically, ARF during sepsis has been considered to be a consequence of diminished renal blood flow (RBF). Indeed, in early stages of sepsis or in sepsis associated to cardiogenic shock, RBF may decrease. However, recent studies have shown that in resuscitated sepsis, in which cardiac output is characteristically normal or even elevated and there is systemic vasodilatation, RBF is normal or even increased, with no associated histological evidence of significant tubular necrosis. Thus, other factors may participate in the genesis of ARF in sepsis. These include apoptosis, glomerular and medullary microcirculatory disorders, cell changes in response to the pro-inflammatory cascade characteristic of sepsis, oxidative stress, mitochondrial dysfunction and damage induced by mechanical ventilation, among others. Sepsis associated ARF treatment is supportive. In general, renal replacement therapies can be grouped as intermittent or continuous, and as those whose primary objective is the replacement of impaired renal function, versus those whose main objective is to secure hemodynamic stability through the clearing of pro-inflammatory mediators.
authors.affiliation: Departamento de Medicina Intensiva, Hospital Clínico Universidad Católica de Chile, Pontificia Universidad Católica de Chile, Santiago, Chile. regueira@med.puc.cl
authors.forename: T
authors.initials: T
authors.lastname: Regueira
authors.forename: M
authors.initials: M
authors.lastname: Andresen
authors.forename: M
authors.initials: M
authors.lastname: Mercado
authors.forename: P
authors.initials: P
authors.lastname: Downey
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000209:etiology / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D017209:Apoptosis; D002302:Cardiac Output; D003404:Creatinine / Q000097:blood; D005919:Glomerular Filtration Rate; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007511:Ischemia / Q000209:etiology / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000473:pathology; D008833:Microcirculation; D008928:Mitochondria / Q000502:physiology; D018384:Oxidative Stress; D012079:Renal Circulation; D017582:Renal Replacement Therapy; D012121:Respiration, Artificial / Q000009:adverse effects; D018805:Sepsis / Q000150:complications*; D019851:Thrombophilia / Q000209:etiology; D014664:Vasodilation
chemical_list: D018836:Inflammation Mediators; D003404:Creatinine