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

Tomás Regueira, Max Andresen, Marcelo Mercado, Felipe Lillo, Dagoberto Soto

Resultado de la investigación: Article

Resumen

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.

Idioma originalSpanish
Páginas (desde-hasta)551-558
Número de páginas8
PublicaciónRevista Medica de Chile
Volumen142
N.º5
DOI
EstadoPublished - 2014

Huella dactilar

Acute Kidney Injury
Sepsis
Kidney
Renal Circulation
Lactic Acid
Histology
Necrosis
Perfusion
Parenteral Infusions
Renal Plasma Flow
Pressure
Inulin
Renal Artery
Vasoconstriction
Feces
Pulmonary Artery
Interleukin-6
Creatinine
Arterial Pressure
Theoretical Models

ASJC Scopus subject areas

  • Medicine(all)

Citar esto

Regueira, Tomás ; Andresen, Max ; Mercado, Marcelo ; Lillo, Felipe ; Soto, Dagoberto. / Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental. En: Revista Medica de Chile. 2014 ; Vol. 142, N.º 5. pp. 551-558.
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Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental. / Regueira, Tomás; Andresen, Max; Mercado, Marcelo; Lillo, Felipe; Soto, Dagoberto.

En: Revista Medica de Chile, Vol. 142, N.º 5, 2014, p. 551-558.

Resultado de la investigación: Article

TY - JOUR

T1 - Determinantes precoces en el desarrollo de injuria renal aguda durante la sepsis abdominal experimental

AU - Regueira, Tomás

AU - Andresen, Max

AU - Mercado, Marcelo

AU - Lillo, Felipe

AU - Soto, Dagoberto

PY - 2014

Y1 - 2014

N2 - 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.

AB - 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.

KW - Acute kidney injury

KW - Renal circulation

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