Introduction (Article introduction authored by ICU Editorial Team) Sepsis, a severe response to infection, can result in life-threatening organ dysfunction, with sepsis-associated acute kidney injury (SA-AKI) being the most common, contributing to approximately 50% of all cases of acute kidney injury (AKI) in critically ill adults. Despite advancements in understanding clinical risk factors, pathobiology, and treatment responses for SA-AKI, it continues to pose a significant health burden. This review explores current treatment standards and recent developments in the pathophysiology, diagnosis, outcome prediction, and management of SA-AKI. Sepsis-associated AKI, affecting up to 60% of sepsis patients, involves intricate mechanisms such as inflammation, complement activation, mitochondrial dysfunction, and microcirculatory dysfunction. The heightened mortality risk associated with AKI in sepsis emphasizes the urgent need for ongoing research aimed at mitigating both short-term and long-term consequences. From diagnosis to treatment of SA-AKI In suspected cases of sepsis, lactate levels should be measured initially, and if elevated (>2 mmol/L), the measurement should be repeated to guide resuscitation based on lactate levels. Once sepsis is confirmed, treatment should adhere to current sepsis guidelines. It is crucial to obtain blood cultures before initiating antibiotic therapy. For patients with sepsis-induced hypoperfusion (lactate levels ≥2 mmol/L) or septic shock, initiate crystalloid fluid administration guided by dynamic parameters of fluid responsiveness. Vasopressors, with norepinephrine recommended as the first-line agent, should be administered to maintain a mean arterial pressure (MAP) >65 mmHg and reduce serum lactate levels. Dopamine is not recommended for use in septic patients. This protocol ensures a systematic and evidence-based approach to managing sepsis and its complications. The article also introduces a diagnostic and treatment algorithm for sepsis-associated acute kidney injury (SA-AKI) in adults, aligned with recent recommendations from the Acute Disease Quality Initiative group. Early fluid administration is critical in sepsis to support both macro- and microcirculation. Guidelines recommend an initial 30 ml/kg of crystalloids, but fluid administration should be individualized based on fluid responsiveness to prevent volume overload. There has been debate regarding the choice of fluid type, particularly 0.9% saline, but recent studies suggest its safe use up to 4 liters. All sepsis patients, especially those with comorbidities like chronic kidney disease, are considered at high risk for acute kidney injury (AKI). Monitoring kidney function using serum creatinine and urine output is essential, although the KDIGO definition of AKI has limitations. Early detection of kidney damage is crucial, and combining markers of damage and function may improve sensitivity and specificity. Biomarkers such as cystatin C, proenkephalin, TIMP2, IGFBP7, and plasma neutrophil gelatinase-associated lipocalin can aid in detecting AKI. Bedside Doppler ultrasound can assess renal perfusion, and the renal resistive index (RRI) may predict AKI. However, Doppler ultrasound may not distinguish patterns of renal recovery. Urinalysis and urine microscopy, particularly evaluation of cast elements and tubule epithelial cells, contribute to identifying sepsis-associated AKI. Together, these tools enhance early detection and monitoring of AKI in septic patients.
