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Circulating pro-apoptotic mediators in burn septic acute renal failure

The pathogenesis of septic acute kidney injury (AKI) is not well understood. In the present issue of Critical Care, the combined clinical and experimental study from Mariano's group provides new insight into the disease. The study shows that plasma from septic burn patients with acute renal fai...

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Autor principal: Oudemans-van Straaten, Heleen M
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447548/
https://www.ncbi.nlm.nih.gov/pubmed/18394180
http://dx.doi.org/10.1186/cc6798
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author Oudemans-van Straaten, Heleen M
author_facet Oudemans-van Straaten, Heleen M
author_sort Oudemans-van Straaten, Heleen M
collection PubMed
description The pathogenesis of septic acute kidney injury (AKI) is not well understood. In the present issue of Critical Care, the combined clinical and experimental study from Mariano's group provides new insight into the disease. The study shows that plasma from septic burn patients with acute renal failure initiated pro-apoptotic effects and functional alterations in renal tubular cells and podocytes in vitro that correlated with the degree of proteinuria and renal dysfunction. Pro-apoptotic effects were not attributable to antibiotic or uremic toxicity, but were partially attributable to endotoxin. Sepsis and burn had additive effects. Apart from increasing our understanding of the pathogenesis of septic AKI, the study justifies further research on therapeutic interventions in several directions. These include the binding and elimination of the source of endotoxin by selective decontamination of the digestive tract, the blocking of apoptotic pathways, or the extracorporeal removal of circulating toxic mediators using high permeability hemofiltration or coupled plasma filtration and absorption.
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spelling pubmed-24475482008-07-10 Circulating pro-apoptotic mediators in burn septic acute renal failure Oudemans-van Straaten, Heleen M Crit Care Commentary The pathogenesis of septic acute kidney injury (AKI) is not well understood. In the present issue of Critical Care, the combined clinical and experimental study from Mariano's group provides new insight into the disease. The study shows that plasma from septic burn patients with acute renal failure initiated pro-apoptotic effects and functional alterations in renal tubular cells and podocytes in vitro that correlated with the degree of proteinuria and renal dysfunction. Pro-apoptotic effects were not attributable to antibiotic or uremic toxicity, but were partially attributable to endotoxin. Sepsis and burn had additive effects. Apart from increasing our understanding of the pathogenesis of septic AKI, the study justifies further research on therapeutic interventions in several directions. These include the binding and elimination of the source of endotoxin by selective decontamination of the digestive tract, the blocking of apoptotic pathways, or the extracorporeal removal of circulating toxic mediators using high permeability hemofiltration or coupled plasma filtration and absorption. BioMed Central 2008 2008-03-31 /pmc/articles/PMC2447548/ /pubmed/18394180 http://dx.doi.org/10.1186/cc6798 Text en Copyright © 2008 BioMed Central Ltd
spellingShingle Commentary
Oudemans-van Straaten, Heleen M
Circulating pro-apoptotic mediators in burn septic acute renal failure
title Circulating pro-apoptotic mediators in burn septic acute renal failure
title_full Circulating pro-apoptotic mediators in burn septic acute renal failure
title_fullStr Circulating pro-apoptotic mediators in burn septic acute renal failure
title_full_unstemmed Circulating pro-apoptotic mediators in burn septic acute renal failure
title_short Circulating pro-apoptotic mediators in burn septic acute renal failure
title_sort circulating pro-apoptotic mediators in burn septic acute renal failure
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447548/
https://www.ncbi.nlm.nih.gov/pubmed/18394180
http://dx.doi.org/10.1186/cc6798
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