Acute renal injury (AKI) occurs in 19% of patients with sepsis, 23% of those with severe sepsis and up to 50% of patients with septic shock. AKI represents an independent prognostic factor of mortality (about 45%); epidemiological studies have pointed out that the onset of AKI in sepsis (S-AKI) correlates with an unfavourable outcome, reaching a mortality of 75%.
Over the years, efforts have been made to prevent and treat “low flow” hemodynamic damage resulting from shock by increasing renal blood flow, improving cardiac output and perfusion pressure. New experimental studies in S-AKI have shown that renal blood flow is maintained, and indeed increases, in the course of septic shock. Recently, a “single theory” has been proposed that defines acute renal injury as the final result of the interaction between inflammation, oxidative stress, apoptosis, microcirculatory dysfunction and the adaptive response of tubular epithelial cells to the septic insult.
The type of treatment, the dose and the starting time of RRT are of strategic importance in the recovery of AKI in septic patients.
The use of new anticoagulation strategies in critically ill patients with S-AKI has allowed treatments to be carried out for enough time to reach the correct dose of purification prescribed, minimizing down-time and bleeding risk.
The availability of new technologies allows to customize treatments more and more; the collaboration between nephrologists and intensivists must always increase in order to implement modern precision medicine in critical care.
Keywords: S-AKI, septic shock, CRRT, citrate, CPFA, adsorption