Physiological aspects of Toll-like receptor 4 activation in sepsis-induced acute kidney injury.

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acute kidney injury 5 nephrologydiseases
chronic kidney disease 2 nephrologydiseases
glomerulonephritis 1 nephrologydiseases
kidney failure 1 nephrologydiseases

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acute kidney injury 121 Physiologica (Oxford, England)Physiological aspects of Toll‐like receptor 4 activation in sepsis‐induced acute kidney injury Alternative Title: S B Anderberg et al.S. B. AnderbergT. LutherR. Frithiof1Department of Surgical SciencesSection of
acute kidney injury 413 UniversityUppsalaSwedenPublication date (epub): 10/2016Publication date (ppub): 3/2017AbstractAbstractSepsis‐induced acute kidney injury (SI‐AKI) is common and associated with high mortality. Survivors are at increased risk of chronic
acute kidney injury 2702 and death. In this review, we explore how one specific TLR, Toll‐like receptor 4 (TLR4), may cause acute kidney injury (AKI) in sepsis. Although many TLRs have been described, TLR4 is so far the most extensively studied.
acute kidney injury 10901 dysfunction in addition to altered renal metabolism and circulation (not shown in figure), giving rise to acute kidney injury . The two methods of inhibiting TLR4 signalling are shown above. Eritoran (E5564), a synthetic lipopolysaccharide,
acute kidney injury 26978 not a morphological problem.Renal macrocirculatory alterations as cause of SI‐AKISepsis‐induced acute kidney injury (SI‐AKI) has traditionally been viewed as a result of hypoperfusion due to distributional hypovolemia
chronic kidney disease 525 injury (SI‐AKI) is common and associated with high mortality. Survivors are at increased risk of chronic kidney disease . The precise mechanism underlying SI‐AKI is unknown, and no curative treatment exists. Toll‐like
chronic kidney disease 8776 5% of hospitalized patients suffer from AKI and thus have an increased risk of dying or developing chronic kidney disease (Wonnacott et al. 2014). In intensive care, AKI is more common and affects more than 50% of the patients
glomerulonephritis 6706 from, that is HIV and Influenza virusTLR7 has been shown to activate B‐lymphocytes and contribute to glomerulonephritis in response to viral agonists (Pawar et al. 2007). Although not verified to be mediated completely
kidney failure 13308 to the hypothesis that local renal and/or systemic inflammation contributes to SI‐AKI and that the kidney failure often seen in association with sepsis not necessarily has to involve inadequate global renal perfusion

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