Sepsis-associated acute kidney injury

Abstract

Acute kidney injury (AKI) is an epidemic problem. Sepsis has long been recognized as a foremost precipitant of AKI. Sepsis-associated AKI (SA-AKI) portends a high burden of morbidity and mortality in both children and adults with critical illness. Although our understanding of its pathophysiology is incomplete, SA-AKI likely represents a distinct subset of AKI contributed to by a unique constellation of hemodynamic, inflammatory, and immune mechanisms. SA-AKI poses significant clinical challenges for clinicians. To date, no singular effective therapy has been developed to alter the natural history of SA-AKI. Rather, current strategies to alleviate poor outcomes focus on clinical risk identification, early detection of injury, modifying clinician behavior to avoid harm, early appropriate antimicrobial therapy, and surveillance among survivors for the longer-term sequelae of kidney damage. Recent evidence has confirmed that patients no longer die with AKI, but from AKI. To improve the care and outcomes for sufferers of SA-AKI, clinicians need a robust appreciation for its epidemiology and current best-evidence strategies for prevention and treatment.

Keywords: acute kidney injury; critical care nephrology; outcomes; sepsis.

Figure 1

Sepsis and AKI pathophysiological interaction in SA-AKI. Reprinted with permission from Romanovsky et al.

Figure 2

Porcine sepsis model does not show renal tubular necrosis. In a porcine model of fecal peritonitis, representative histopathologic cross-sections of renal tubules shows tubular vacuolization, a precursor of cellular apoptosis, but no evidence of necrosis. (A) Representative histologic image of a control kidney. (B) Representative histologic image of a septic kidney. Arrows show epithelial vacuolization with damage of brush border. Reproduced with permission from Chvojka et al.