Management of AKI: Vasopressors

The maintenance of normal renal function relies on adequate renal perfusion pressure, which is determined by the difference between mean arterial pressure and central venous pressure. Hypotension stands out as a primary determinant of acute kidney injury (AKI), particularly following surgical procedures. In cases where mean arterial pressure targets cannot be reached through fluid therapy alone, vasopressors and inotropic agents become necessary to enhance kidney microcirculation. Before initiating these medications, it is essential to assess and optimize intravascular volume status. The choice of the initial agent should align with the suspected underlying cause of shock and AKI, whether it be sepsis, hepatorenal syndrome, cardiac failure, anaphylaxis, or others. Exogenous dopamine, norepinephrine, and epinephrine exert sympathomimetic effects on alpha- and beta-adrenergic receptors, resulting in heightened vascular tone and increased cardiac output. Vasopressin and angiotensin II, natural hormones, along with terlipressin, a vasopressin analog, have been proposed as adjunctive therapy for vasodilatory conditions due to their non-catecholaminergic vasopressor effects. However, current clinical evidence is insufficient to determine whether one vasoactive agent surpasses others in the prevention or treatment of AKI. This chapter delves into the pathophysiology of renal perfusion disorders and provides insights into the indications and contraindications of vasopressors within the context of AKI.