Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental

Background: Sepsis-induced acute kidney injury (AKI) is an early and frequent organ dysfunction, associated with increased mortality. Aim: To evaluate the impact of macrohemodynamic and microcirculatory changes on renal function and histology during an experimental model of intra-abdominal sepsis. M...

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Autores principales:	Regueira,Tomás, Andresen,Max, Mercado,Marcelo, Lillo,Felipe, Soto,Dagoberto
Lenguaje:	Spanish / Castilian
Publicado:	Sociedad Médica de Santiago 2014
Materias:	Acute kidney injury Renal circulation Sepsis
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872014000500001
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spelling	oai:scielo:S0034-988720140005000012014-10-10Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimentalRegueira,TomásAndresen,MaxMercado,MarceloLillo,FelipeSoto,Dagoberto Acute kidney injury Renal circulation Sepsis Background: Sepsis-induced acute kidney injury (AKI) is an early and frequent organ dysfunction, associated with increased mortality. Aim: To evaluate the impact of macrohemodynamic and microcirculatory changes on renal function and histology during an experimental model of intra-abdominal sepsis. Material and Methods: In 18 anaesthetized pigs, catheters were installed to measure hemodynamic parameters in the carotid, right renal and pulmonary arteries. After baseline assessment and stabilization, animals were randomly divided to receive and intra-abdominal infusion of autologous feces or saline. Animals were observed for 18 hours thereafter. Results: In all septic animals, serum lactate levels increased, but only eight developed AKI (66%). These animals had higher creatinine and interleukin-6 levels, lower inulin and para-aminohippurate clearance (decreased glomerular filtration and renal plasma flow), and a negative lactate uptake. Septic animals with AKI had lower values of mean end arterial pressure, renal blood flow and kidney perfusion pressure, with an associated increase in kidney oxygen extraction. No tubular necrosis was observed in kidney histology. Conclusions: The reduction in renal blood flow and renal perfusion pressure were the main mechanisms associated with AKI, but were not associated with necrosis. Probably other mechanisms, such as microcirculatory vasoconstriction and inflammation also contributes to AKI development.info:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.142 n.5 20142014-05-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872014000500001es10.4067/S0034-98872014000500001
institution	Scielo Chile
collection	Scielo Chile
language	Spanish / Castilian
topic	Acute kidney injury Renal circulation Sepsis
spellingShingle	Acute kidney injury Renal circulation Sepsis Regueira,Tomás Andresen,Max Mercado,Marcelo Lillo,Felipe Soto,Dagoberto Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
description	Background: Sepsis-induced acute kidney injury (AKI) is an early and frequent organ dysfunction, associated with increased mortality. Aim: To evaluate the impact of macrohemodynamic and microcirculatory changes on renal function and histology during an experimental model of intra-abdominal sepsis. Material and Methods: In 18 anaesthetized pigs, catheters were installed to measure hemodynamic parameters in the carotid, right renal and pulmonary arteries. After baseline assessment and stabilization, animals were randomly divided to receive and intra-abdominal infusion of autologous feces or saline. Animals were observed for 18 hours thereafter. Results: In all septic animals, serum lactate levels increased, but only eight developed AKI (66%). These animals had higher creatinine and interleukin-6 levels, lower inulin and para-aminohippurate clearance (decreased glomerular filtration and renal plasma flow), and a negative lactate uptake. Septic animals with AKI had lower values of mean end arterial pressure, renal blood flow and kidney perfusion pressure, with an associated increase in kidney oxygen extraction. No tubular necrosis was observed in kidney histology. Conclusions: The reduction in renal blood flow and renal perfusion pressure were the main mechanisms associated with AKI, but were not associated with necrosis. Probably other mechanisms, such as microcirculatory vasoconstriction and inflammation also contributes to AKI development.
author	Regueira,Tomás Andresen,Max Mercado,Marcelo Lillo,Felipe Soto,Dagoberto
author_facet	Regueira,Tomás Andresen,Max Mercado,Marcelo Lillo,Felipe Soto,Dagoberto
author_sort	Regueira,Tomás
title	Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
title_short	Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
title_full	Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
title_fullStr	Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
title_full_unstemmed	Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
title_sort	determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental
publisher	Sociedad Médica de Santiago
publishDate	2014
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872014000500001
work_keys_str_mv	AT regueiratomas determinantesprecoceseneldesarrollodeinjuriarenalagudadurantelasepsisabdominalexperimental AT andresenmax determinantesprecoceseneldesarrollodeinjuriarenalagudadurantelasepsisabdominalexperimental AT mercadomarcelo determinantesprecoceseneldesarrollodeinjuriarenalagudadurantelasepsisabdominalexperimental AT lillofelipe determinantesprecoceseneldesarrollodeinjuriarenalagudadurantelasepsisabdominalexperimental AT sotodagoberto determinantesprecoceseneldesarrollodeinjuriarenalagudadurantelasepsisabdominalexperimental
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Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental

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