Hemodynamic management of acute kidney injury

To discuss the role of hemodynamic management in critically ill patients with acute kidney injury.

Acute kidney injury (AKI) may be associated with persistent alterations in renal perfusion, even when cardiac output and blood pressure are preserved. The effects of interventions aiming at increasing renal perfusion are best evaluated by renal Doppler or contrast enhance ultrasound. However, limited data have been acquired with these techniques and the essential of the literature is based on surrogates of renal function such as incidence of use of renal replacement therapy. Fluids may increase renal perfusion but their effects are quite unpredictable and can be dissociated from their impact on cardiac output and arterial pressure. Inotropes can also be used in selected conditions. At the de-escalation phase, fluid withdrawal should be considered. Safe fluid withdrawal may be achieved when applied in selected patients with preserved tissue perfusion presenting signs of fluid intolerance. When applied, stopping rules should be set. Dobutamine, milrinone and levosimendan increase renal perfusion in AKI associated with cardiac failure or after cardiac surgery. However, the impact of these agents in sepsis is not well defined. Regarding vasopressors, norepinephrine is the first-line vasopressor agent, but vasopressin derivative may limit the requirement of renal replacement therapy. Angiotensin has promising effects in a limited size post-Hoc analysis of a RCT, but these data need to be confirmed. While correction of severe hypotension is associated with improved renal perfusion and function, the optimal mean arterial pressure (MAP) target level remains undefined, Systematic increase in MAP results in variable changes in renal perfusion. It sounds reasonable to individualize MAP target, paying attention to central venous and intraabdominal pressures, as well as to the response to an increase in MAP.

Recent studies have refined the impact of the various hemodynamic interventions on renal perfusion and function in critically ill patients with AKI. Though several of these interventions improve renal perfusion, their impact on renal function is more variable.