The Role of suPAR in Kidney Injury Progression

This article provides a thorough review of how suPAR influences kidney injury. It aims to inform relevant fields, clarify the mechanisms of its effects, and ultimately enhance patient treatment outcomes and quality of life.

A thorough literature review was conducted, analyzing published research articles, meta-analyses, and clinical studies investigating the structure, function, and pathophysiological roles of suPAR in various forms of kidney injury. Mechanisms were explored through evidence from in vitro studies, animal models, and human observational/clinical trials. The focus was on suPAR's involvement in key processes like inflammation, oxidative stress, apoptosis, and fibrosis within the kidney.

suPAR drives AKI progression by promoting inflammation (via NF-κB/NLRP3 activation), oxidative stress (via ROS generation), and apoptosis. In CKD, suPAR induces podocyte injury (via αvβ3 integrin/Rac1 signaling) and renal fibrosis. Elevated suPAR levels predict AKI incidence and CKD progression. suPAR also mediates AKIto- CKD transition.

suPAR is an important pathogenic mediator in kidney injury. In Acute Kidney Injury (AKI), suPAR drives progression via inflammation, oxidative stress, and apoptosis. In Chronic Kidney Disease (CKD), it promotes renal fibrosis. Furthermore, suPAR facilitates the transition from AKI to CKD.

suPAR is a critical pathogenic factor and biomarker driving kidney injury progression in AKI (via inflammation/oxidative stress/apoptosis) and CKD (via fibrosis), and facilitates the AKI-to-CKD transition.