Aguilar Martin Gerardo, AlHussen Hassen A, Gandhi Prenika Devadas, Kaur Priyadeep, Pothacamuri Mounica A, Talikoti Mariam Altaf Husain, Avula Nandita, Shekhawat Pallavi, Silva Alisson Barbosa, Kaur Arshpreet, Rai Manju
Internal Medicine, Garci︠a PCP Universidad de Durango Campus Ciudad Jua︠rez, Chihuahua, MEX.
Critical Care Medicine, Sulieman Alhabib Medical Academy, Riyadh, SAU.
Cureus. 2024 Dec 19;16(12):e75992. doi: 10.7759/cureus.75992. eCollection 2024 Dec.
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.
脓毒症相关急性肾损伤(S-AKI)是一种严重并发症,对脓毒症患者的发病率和死亡率有显著影响。本叙述性综述探讨了S-AKI复杂且多因素的病理生理学,其涉及血流动力学改变、微循环功能障碍、内皮损伤、炎症反应、氧化应激和肾小管直接损伤。将S-AKI主要与肾血流量减少联系起来的传统观点现在正被重新审视,越来越多的见解强调微循环功能障碍和内皮激活作为关键因素的重要性。该综述还讨论了S-AKI目前的诊断方法,强调了现有生物标志物的局限性以及对更早、更准确检测方法的需求。标准治疗策略侧重于支持性治疗,包括液体管理、血管升压药治疗和肾脏替代治疗。然而,这些方法往往无法解决S-AKI的潜在机制,导致死亡率持续居高不下。新兴疗法,包括使用抗氧化剂、抗炎药和基于干细胞的治疗方法,有望改善治疗结果。这些创新方法旨在在分子水平上针对病理生理过程,为更好地管理S-AKI带来希望。该综述强调需要持续开展研究,以进一步了解驱动S-AKI的机制,并制定更有效的治疗策略。