Sepsis accounts for up to one-half of AKI cases in developed countries1. Although sepsis-mediated hypoperfusion causing tubular necrosis has traditionally been implicated as the primary basis for SA-AKI, an increasing number of studies have suggested that SA-AKI is a distinct subset of AKI differentiated from other causes by unique hemodynamic and inflammatory/immune-related mechanisms.
Many animal and limited human studies have found that renal blood flow is an inconsistent predictor of SA-AKI unless cardiac output is affected1, possibly related to the redistribution of blood in the renal microvasculature to the detriment of the renal cortex in sepsis2.
Cytokine-mediated response in sepsis can also lead to tubular cellular injury without necessarily causing necrosis. Of interest, an autopsy study found histological features of acute tubular necrosis in only 22% of patients with clinical diagnosis of SA-AKI 3.
Differences in its pathophysiology may at least in part explain why oliguria, renal function recovery, hemodialysis and death are more common among SA-AKI patients4.
- Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM. Sepsis-associated acute kidney failure. Semin Nephrol 2015;35:2-11.
- Zafrani L, Payen D, Azoulay E, Ince C. The microcirculation of the septic kidney. Semin Nephrol 2015;35:75-84.
- Langenberg C, Bagshaw SM, May CN, Bellomo R. The histopathology of septic acute kidney injury: a systemic review. Crit Care 2008;12:R38.
- Cruz MG, de Oliveira Dantas JGA, Levi TM, et al. Septic versus non-septic acute kidney injury in critically ill patients: characteristics and clinical outcome. Rev Bras Ter Intensiva 2014;26:384-391.