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, possibly related to the redistribution of blood in the renal microvasculature to the detriment of the renal medulla 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.

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References

1. Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM. Sepsis-associated acute kidney failure. Semin Nephrol 2015;35:2-11.  https://www.ncbi.nlm.nih.gov/pubmed/25795495
2. Maiden MJ, Otto S, Brealey JK, et al. Structure and function of the kidney in septic shock. Am J Resp Crit Care Med 2016;194:692-700. https://www.atsjournals.org/doi/abs/10.1164/rccm.201511-2285OC
3. Langenberg C, Bagshaw SM, May CN, Bellomo R. The histopathology of septic acute kidney injury: a systemic review. Crit Care 2008;12:R38.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447560/
4. 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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304467/