suggest a MAP target of 65 mmHg [8]. However, some authors propose that intensive care unit (ICU) patients with sepsis may face the risk of AKI even with a MAP of 85 mmHg [9]. Furthermore, in chronically hypertensive patients, a higher MAP target may prove beneficial [10]. Adequate intravascular volume resuscitation, vasopressors, and inotropic agents constitute the cornerstone of optimizing renal hemodynamics [3]. Crystalloids represent the first-line therapy in hypotensive patients, with balanced solutions preferred over 0.9% saline due to the risk of AKI progression and the need for renal replacement therapy [ overload exacerbates renal oxygenation [14] and may compromise renal function and patient survival [ systemic vascular resistance, such as severe pancreatitis, anaphylaxis, burns, and liver failure, renal autoregulation is disrupted. Persistent hypotension, despite intra­vascular volume optimization, places patients at risk for AKI development [17]. In sepsis, renal damage develops because of endothelial cell injury, impaired intercellular communication, glycocalyx shedding, coagulation dysfunction, leuko­cyte and platelet adhesion, and microthrombosis [ despite adequate RPP. When MAP targe ts cannot be achieved solely with fluid therapy, vasopressors and inotropic agents are employed to enhance kidney micro­circulation. The sympathomimetic effects on alpha- and beta-adrenergic receptors of exogenous dopamine, norepinephrine, and epinephrine result in increased vascular tone and cardiac output (CO) [17]. Vasopressin and angiotensin II, two naturally occurring hormones, along with terlipressin, a vasopressin analog, have been suggested as adjunctive treatments for vasodilatory states, owing to their non­catecholaminergic vasopressor effect [ excessive renal arterial vasoconstriction remains narrow and subject to debate [20]. Notably, some studies propose that exposure to catecholamines may be detri­mental to renal function [