Sepsis-Associated Acute Kidney Injury: Pathophysiology and Treatment Modalities

Sepsis-associated acute kidney injury (S-AKI) is a critical complication that significantly contributes to the morbidity and mortality of sepsis patients. This narrative review explores the complex and multifactorial pathophysiology of S-AKI, which involves hemodynamic alterations, microcirculatory dysfunction, endothelial damage, inflammatory responses, oxidative stress, and direct tubular injury. Conventional perspectives linking S-AKI primarily to reduced renal blood flow are now being reconsidered, with growing insights highlighting the significance of microcirculatory dysfunction and endothelial activation as key contributors. The review also discusses the current diagnostic approaches for S-AKI, emphasizing the limitations of existing biomarkers and the need for earlier and more accurate detection methods. Standard treatment strategies focus on supportive care, including fluid management, vasopressor therapy, and renal replacement therapy. However, these approaches often fail to address the underlying mechanisms of S-AKI, resulting in persistently high mortality rates. Emerging therapies, including the use of antioxidants, anti-inflammatory agents, and stem cell-based treatments, offer the potential for improved outcomes. These innovative approaches aim to target the pathophysiological processes at the molecular level, offering hope for better management of S-AKI. The review highlights the need for ongoing research to further understand the mechanisms driving S-AKI and to develop more effective therapeutic strategies.