AKI can result from reduced kidney perfusion. Renal blood flow (RBF) is deter­mined by the pressure gradient between inflow and outflow pressures in the kidneys (ΔP), as well as vascular resistance (R), RBF = [ΔP/R]. The inflow pressure depends on mean arterial pressure (MAP), while the outflow pressure is influenced by the renal venous pressure. Hypotension decreases RBF by reducing inflow pressure. Conversely, an increase in outflow pressure, often seen in systemic venous congestion due conditions like right heart failure, cirrhosis, or compartment syn­drome, can lead to interstitial edema and increased resistance to RBF. Resistance is chiefly determined by the afferent and efferent arterioles. Vasoconstriction of both arterioles reduces RBF, while efferent arteriolar vasoconstriction increases the glomerular capillary pressure and filtration fraction [ ible, persistent renal ischemia leads to an acute tubular necrosis (ATN) with tubular epithelial injury, cell death, and delayed renal recovery, necessitating tissue regen­eration [13, 14]. Furthermore, multiple inflammatory mechanisms contribute to AKI’s pathogenesis, involving direct cellular injury, inflammation-induced damage, and microcirculatory system alterations [ 15].Given the interplay of local and systemic inflammation, changes in intrarenal blood flow, and microcirculatory dysfunction, improving calculated renal oxygen delivery through systemic circula­tion alone may not easily reverse these processes. In this setting, the main physio­logical rationale for administration of fluids in critically ill patients with AKI is to increase stroke volume (SV) and, consequently, cardiac output (CO) to optimize systemic blood flow and tissue perfusion, to reverse renal ischemia, and to avert the onset of ATN [ diuresis, dilute tubular toxins, and attenuate tubular obstruction in the renal tubules and correct electrolyte alterations and acid-base disorders. In clinical practice, no single clinical or laboratory marker can be used to quantify renal perfusion.