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

• Tomás Regueira ^[1] ; Max Andresen ^[1] ; Marcelo Mercado ^[1] ; Felipe Lillo ^[2] ; Dagoberto Soto ^[1]
  1. [1] Pontificia Universidad Católica de Chile

     Pontificia Universidad Católica de Chile

     Santiago, Chile

     
  2. [2] Universidad Andrés Bello

     Universidad Andrés Bello

     Santiago, Chile

     
• Localización: Revista Médica de Chile, ISSN-e 0034-9887, Vol. 142, Nº. 5, 2014, págs. 551-558
• Idioma: español
• Títulos paralelos:
  • Early determinants of acute kidney injury during experimental intra-abdominal sepsis
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• 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.