Pathobiology of Acute Kidney Injury

Dear Colleagues,

Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal parenchymal cells (endothelial and epithelial) resulting in the onset of AKI. Furthermore, the pathogenesis of kidney injury following AKI involves a complex interaction between altered microcirculatory hemodynamics, renal parenchymal cells, and infiltrating innate and adaptive immune cells. Considerable data support that the immune system mediates AKI, yet many of the underlying mechanisms still remain unclear. Furthermore, lack of clinical data supporting the involvement of the immune system in AKI pathogenesis have hindered the development of clinically tenable anti-inflammatory options. Therefore, as of now, dialysis remains the only treatment option available to AKI patients, underscoring the need to develop novel approaches to tackle this hurdle to ultimately improve patient quality of life. Thus, in order to better understand these comlexities of AKI, it is necessary to clarify these interplays. In this Special Issue on “Pathobiology of Acute Kidney Injury”, we will discuss various mediators of inflammation to further understand their interactions that result in AKI. 

Dr. Amandeep Bajwa
Dr. Navjot Pabla
Guest Editors

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