Acute kidney injury (AKI) is common in the setting of shock. Hemodynamic instability is a risk factor for the development of AKI, and pathophysiological mechanisms include loss of renal perfusion pressure and impaired microcirculation. Although restoration of mean arterial pressure (MAP) may mitigate the risk of AKI to some extent, evidence on this is conflicting. Also debatable is the optimal blood pressure needed to minimize the risk of kidney injury. A MAP of 65 mm Hg traditionally has been considered adequate to maintain renal perfusion pressure, and studies have failed to consistently show improved outcomes at higher levels of MAP. Therapeutic options to support renal perfusion consist of catecholamines, vasopressin, and angiotensin II. Although catecholamines are the most studied, they are associated with adverse events at higher doses, including AKI. Vasopressin and angiotensin II are noncatecholamine options to support blood pressure and may improve microcirculatory hemodynamics through unique mechanisms, including differential vasoconstriction of efferent and afferent arterioles within the nephron. Future areas of study include methods by which clinicians can measure renal blood flow in a macrocirculatory and microcirculatory way, a personalized approach to blood pressure management in septic shock using patient-specific measures of perfusion adequacy, and novel agents that may improve the microcirculation within the kidneys without causing adverse microcirculatory effects in other organs.