Clinical issues and pathophysiology of septic acute kidney injury

Abstract

Sepsis is the major cause of acute kidney injury (AKI) in one-third of AKI patients requiring renal replacement therapy (RRT). Septic AKI has high morbidity and high mortality, with the latter being 60％. The annual incidence of AKI requiring RRT is 13.3 per 100,000 people in Japan. Thus, septic AKI is now considered as one of the most important clinical problems especially in intensive care units. Early goal-directed therapy, studies of new biomarkers, and refinement of RRT have been conducted as an attempt to prevent and/or alleviate septic AKI. The pathophysiology of septic AKI is complex and multifactorial. Recent studies have demonstrated strategies targeting vascular permeability, oxidative stress, and inducible nitric oxide synthase (iNOS) that can alleviate septic AKI. In addition, the regulation of Toll-like receptor (TLR) 9, one of TLRs starting innate immunity, has been reported to improve septic AKI and mortality through avoidance of immune suppression. This review provides an update on the pathophysiology of septic AKI with focus on 3 categories: renal hemodynamics, substantial renal injury, and innate immunity.