Objective: To review the unique pathophysiology of sepsis-induced acute kidney injury (AKI) and highlight the relevant aspects of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury that may apply to veterinary patients.
Data Sources: Electronic search of MEDLINE database.
Human Data Synthesis: Sepsis-induced AKI is diagnosed in up to 47% of human ICU patients and is seen as a major public health concern associated with increased mortality and increased progression to chronic kidney disease (CKD). Consensus criteria for the definition and classification of AKI has allowed for accurate description of the epidemiology of patients with AKI. AKI develops from a complex relationship between the initial insult and activation of inflammation and coagulation. In contrast to the traditional view, clinical and experimental data dispute the role of renal ischemia-reperfusion in the development of sepsis-induced AKI. Renal tubular dysfunction with activation of the tubuloglomerular feedback mechanism appears to be a crucial contributor to sepsis-induced AKI. Furosemide and n-acetylcysteine (NAC) do not appear to be helpful in the treatment of AKI. Hydroxyethyl starches (HES), dopamine, and supraphysiological concentrations of chloride are harmful in patients with AKI.
Veterinary Data Synthesis: Community and hospital-acquired AKI is a significant factor affecting survival in critical ill patients. Sepsis-induced AKI occurs in 12% of dogs with abdominal sepsis and is an important contributor to mortality. Early detection of AKI in hospitalized patients currently offers the best opportunity to improve patient outcome. The use of urinary biomarkers to diagnose early AKI should be evaluated in critical care patients.
Conclusion: Veterinary clinical trials comparing treatment choices with the development of AKI are needed to make evidence-based recommendations for the prevention and treatment of AKI.
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