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Noninvasive and Invasive Renal Hypoxia Monitoring in a Porcine Model of Hemorrhagic Shock
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Hemorrhagic shock induces renal complement activation.

Christian Ehrnthaller1,2,3, Anke Schultze4, Gamal Wakileh5,4

  • 1Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, Ulm, Germany. christian.ehrnthaller@med.uni-muenchen.de.

European Journal of Trauma and Emergency Surgery : Official Publication of the European Trauma Society
|July 17, 2019
PubMed
Summary
This summary is machine-generated.

Complement activation occurs during hemorrhagic shock, impacting kidney injury. This study found diminished zonulin levels correlated with complement changes, suggesting their role in acute kidney failure following shock.

Keywords:
Acute kidney failureComplementHemorrhagic shockTight junctionZonulin

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Area of Science:

  • Immunology
  • Pathophysiology
  • Renal Medicine

Background:

  • Complement activation is implicated in hemorrhagic shock.
  • The role of complement in local tissue damage and organ failure remains unclear.
  • Zonulin is a known complement activator linked to organ failure.

Purpose of the Study:

  • To investigate local and systemic complement activation during hemorrhagic shock.
  • To examine the consequences of hemorrhagic shock on zonulin levels.
  • To explore the relationship between complement activation, zonulin, and acute kidney injury.

Main Methods:

  • Porcine model of hemorrhagic shock (n=9) with controlled hypotension for 4 hours.
  • Collection of central and renal blood samples at baseline, 4 hours post-hemorrhage, and 12/22 hours post-resuscitation.
  • Analysis of high-mobility group box 1 (HMGB-1), C3a, zonulin, terminal complement complex (TCC), CH50, C3c deposition, and neutrophil gelatinase-associated lipocalin (NGAL).

Main Results:

  • Elevated HMGB-1 in plasma and kidneys post-hemorrhage.
  • Increased central TCC and decreased renal CH50 levels observed.
  • Evidence of local complement activation via C3c deposition in kidneys.
  • Significantly diminished zonulin levels systemically and renally, correlating with CH50 and NGAL.

Conclusions:

  • Central complement activation may lead to complement product consumption in kidney tissue.
  • Diminished zonulin levels suggest its involvement alongside complement in acute kidney failure.
  • Findings highlight the potential roles of complement and zonulin in the pathophysiology of shock-induced kidney injury.