New Insights into the Renal Microcirculation in Sepsis-Induced Acute Kidney Injury

Acute kidney injury (AKI) is a frequent complication during septic shock with the incidence of AKI ranging from 55% to 73% [1–3]. Sepsis-induced AKI is independently associated with mortality [4] and survivors have a greater risk of developing chronic and end-stage kidney disease [5]. Thus, understanding the pathophysiology of sepsis-induced AKI is essential for appropriate treatment. Renal microvascular alterations appear to play a role in the occurrence of septic AKI [6, 7], but the relative contribution of renal microvascular alterations in the pathophysiology of sepsis-induced AKI in septic patients remains to be determined. Indeed, without the possibility of assessment of the renal microcirculation, renal perfusion status remains poorly studied in patients with septic shock. Thus, in clinical practice during the resuscitation of septic shock, physicians hope that optimization of the macrocirculation (i.e., mean arterial pressure [MAP] and systemic oxygen delivery) will be beneficial to the renal microcirculation but are totally blind to the actual behavior of the renal microcirculation. To gain new insights into the pathogenesis of AKI in septic patients and in intensive care unit (ICU) patients, we need new techniques to evaluate kidney microcirculation. In this chapter, we focus on recent results that have clarified the contribution of renal microvascular alterations in sepsis-induced AKI in septic patients. We expect that these findings will improve the understanding and the clinical management (prevention and treatment) of sepsis-induced AKI.