Acute kidney injury (AKI) is a syndrome characterized by the rapid loss of kidney function and is typically diagnosed by an increase in blood-urea-nitrogen and serum creatinine, a decrease in the glomerular filtration rate (GFR), and a decrease in urine output. AKI can be brought on by a myriad of events: physical damage to the kidney, cardiac arrest, blood loss, toxicologic effects from pharmacological drug use, and in most cases seen, sepsis. These events introduce global and or local ischemic insult to the kidney, causing a decrease in renal functionality. Originally, global renal hypoperfusion was thought to be the culprit causing AKI. However, evidence is showing that AKI can occur in the absence of this, proved by the normal or even increased blood flow seen in sepsis-induced AKI. In fact, studies are finding similar results that show microcirculatory dysfunction, inflammation, and tubular oxidative stress are the driving physiological factors for sepsis-induced AKI.
The development and use of intravital video microscopy (IVVM) allows \textit{in vivo} studies of biological systems to be conducted. The excitation and emission of Flourophores are used to visualize specific structures and interactions within a system, and provide the means for analysis. Visualization of renal system structure and dynamics have be captured using IVVM, specifically ATP generation activity seen in the tubular epithelial cells and the microvascular dysfunction of blood flow associated with sepsis-induced AKI. The work proposed here focuses on using these images to quantify and explain the heterogeneity seen in the microhemodynamics of the cortical peritubular capillaries as well as mitochondrial energetics of the renal system. The information learned regarding oxygen delivery and energy consumption can be used to further understand the physio/pathophysio-logical interactions of the renal system in states of health and AKI
