Acute kidney injury (AKI) is a common complication in critically ill patients, especially among septic patients. Sepsis and hypovolemia are the 2 most frequent etiologies of AKI in intensive care units and frequently coexist in critically ill patients. Effective fluid resuscitation is crucial for the stabilization of sepsis-induced tissue hypoperfusion or septic shock. However, the lack of a goal-directed therapy targeting kidney oxygenation prevents from optimization of the fluid therapy with regard to improvement of renal oxygen delivery and extraction. Similarly, fluid administration as all therapeutic actions carries adverse effects such as the activation of cytokines, disruption of the capillary glycocalyx, and adverse effects on kidney metabolism and oxygenation. Moreover, a positive fluid balance is associated with an increased risk of AKI and is a negative predictor for recovery of renal function. The role of fluid resuscitation on kidney injury stems from the high renal vulnerability to hypoxemic injury. Indeed, fluids have a poor oxygen solubility and hemodilution decreases blood viscosity both promoting intrarenal shunting and heterogeneity with a decreased capillary density and enhanced intrarenal cortex and medullary hypoxia. The development of physiological biomarkers that are able to detect the early development of AKI specifically aimed at the identification of renal microcirculatory dysfunctions should form a valuable contribution to monitoring therapeutic modalities.
Acute Kidney Injury and Fluid Resuscitation in Septic Patients: Are We Protecting the Kidney?