Acute Kidney Injury at the Neurocritical Care Unit

Neurocritical care has advanced substantially in recent decades, allowing doctors to treat patients with more complicated conditions who require a multidisciplinary approach to achieve better clinical outcomes. In neurocritical patients, nonneurological complications such as acute kidney injury (AKI) are independent predictors of worse clinical outcomes. Different research groups have reported an AKI incidence of 11.6% and an incidence of stage 3 AKI, according to the Kidney Disease: Improving Global Outcomes, that requires dialysis of 3% to 12% in neurocritical patients. These patients tend to be younger, have less comorbidity, and have a different risk profile, given the diagnostic and therapeutic procedures they undergo. Trauma-induced AKI, sepsis, sympathetic overstimulation, tubular epitheliopathy, hyperchloremia, use of nephrotoxic drugs, and renal hypoperfusion are some of the causes of AKI in neurocritical patients. AKI is the result of a sum of events, although the mechanisms underlying many of them remain uncertain; however, two important causes that merit mention are direct alteration of the physiological brain-kidney connection and exposure to injury as a result of the specific medical management and well-established therapies that neurocritical patients are subjected to. This review will focus on AKI in neurocritical care patients. Specifically, it will discuss its epidemiology, causes, associated mechanisms, and relationship to the brain-kidney axis. Additionally, the use and risks of extracorporeal therapies in this group of patients will be reviewed.