Role of the Renin Angiotensin Aldosterone System in the Pathogenesis of Sepsis-Induced Acute Kidney Injury: A Systematic Review

Figures

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  Figure 1. PRISMA 2020 Flow Diagram for the search and selection of studies.

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  Figure 2. Interplay of Mechanisms in the Development of S-AKI. This figure displays the abundance of pro-inflammatory and coagulative factors present in the renal microvasculature during sepsis. These elements migrate from both systemic and local sources. Endothelial damage by ROS* and cytokines exposes vWF*, which activates platelet aggregation and the coagulation cascade. Having also migrated to the renal circulation, leukocytes, including monocytes and neutrophils, release pro-inflammatory cytokines and leak into extravascular spaces, causing edema. The interplay of these processes contributes to the pathogenesis of S-AKI. *ROS: reactive oxygen species; vWF: von Willebrand Factor. This figure was partly generated using Servier Medical Art, provided by Servier and licensed under a Creative Commons Attribution 3.0 unported license.

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  Figure 3. Role of the RAAS* and RAAS Inhibitors in the Pathophysiology of S-AKI. This schematic representation of the renin angiotensin aldosterone system conveys its key components and main effects on the human body. The role of angiotensin II in inflammation, oxidative stress, and coagulation, which contribute to the development of S-AKI, is also indicated. RAAS inhibitors minimize these processes by modulating ACE* activity and blocking angiotensin II receptors. *RAAS: renin angiotensin aldosterone system; ACE: angiotensin converting enzyme. This figure was partly generated using Servier Medical Art, provided by Servier and licensed under a Creative Commons Attribution 3.0 unported license.