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Updated: Mar 25, 2026

Standardized Colon Ascendens Stent Peritonitis in Rats - a Simple, Feasible Animal Model to Induce Septic Acute Kidney Injury
Published on: February 15, 2022
Pathophysiology of Septic Acute Kidney Injury
Background:
Despite increased understanding of the pathophysiology of septic acute kidney injury (AKI), treatment options are limited, and mortality remains high.
Summary:
Septic AKI is triggered by pathogen-associated molecular patterns from bacteria and damage-associated molecular patterns released from or exposed on damaged cells. Downstream effects include glomerular and peritubular endothelial dysfunction, downregulation of tubular reabsorptive work, cell-cycle arrest, regulated cell death and destruction of damaged cell organelles. In the laboratory, pharmacological modulation of some of these pathways prevents AKI or enhances recovery from AKI, yet no data exist to support the utility of such AKI therapy in man. However, avoiding systemic and renal venous congestion, hypotension and fluid overload attenuates AKI in critically ill septic patients.
Key Message:
While therapies aiming at modulating the sepsis-induced cellular response are discovered and tested, hemodynamic optimization remains critical in patients with or at risk of AKI.
Insights
Treating septic acute kidney injury (AKI) is challenging due to limited options. While lab research shows promise, managing blood flow and fluid balance is key for critically ill patients with sepsis-induced AKI.
Area of Science:
- Nephrology
- Critical Care Medicine
- Immunology
Background:
- Sepsis-induced acute kidney injury (AKI) remains a significant clinical challenge with high mortality rates.
- Despite advances in understanding its pathophysiology, effective therapeutic options for septic AKI are limited.
Purpose of the Study:
- To review the pathophysiology of septic AKI.
- To discuss potential therapeutic targets and current management strategies.
Main Methods:
- Review of current literature on septic AKI.
- Analysis of molecular and cellular pathways involved in septic AKI.
- Evaluation of clinical management strategies.
Main Results:
- Septic AKI involves complex pathways including endothelial dysfunction, tubular damage, and cellular death.
- Experimental therapies targeting these pathways show promise in preclinical models.
- Clinical data supporting these targeted therapies in humans are currently lacking.
Conclusions:
- Septic AKI is initiated by pathogen- and damage-associated molecular patterns, leading to widespread cellular dysfunction.
- While novel therapies are under investigation, hemodynamic optimization, including avoidance of congestion, hypotension, and fluid overload, is critical for managing septic AKI in critically ill patients.
Related Concept Videos
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury I: Introduction
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Pyelonephritis I: Introduction
Acute Kidney Injury III: Clinical Manifestations
Acute Kidney Injury V: Interprofessional Care

