Asset Details
Do you wish to reserve the book?
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
Do you wish to request the book?
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
2025
Overview
Acute kidney injury (AKI) encompasses pathophysiology ranging from glomerular hypofiltration to tubular cell injury and outflow obstruction. This Review will focus on the tubulointerstitial processes that underlie most cases of AKI. Tubular epithelial cell (TEC) injury can occur via distinct insults, including ischemia, nephrotoxins, sepsis, and primary immune-mediated processes. Following these initial insults, tubular cells can activate survival and repair responses or they can develop mitochondrial dysfunction and metabolic reprogramming, cell-cycle arrest, and programmed cell death. Developing evidence suggests that the fate of individual tubular cells to survive and proliferate or undergo cell death or senescence is frequently determined by a biphasic immune response with initial proinflammatory macrophage, neutrophil, and lymphocyte infiltration exacerbating injury and activating programmed cell death, while alternatively activated macrophages and specific lymphocyte subsets subsequently modulate inflammation and promote repair. Functional recovery requires that this reparative phase supports proteolytic degradation of tubular casts, proliferation of surviving TECs, and restoration of TEC differentiation. Incomplete resolution or persistence of inflammation can lead to failed tubular repair, fibrosis, and chronic kidney disease. Despite extensive research in animal models, translating preclinical findings to therapies remains challenging, emphasizing the need for integrated multiomic approaches to advance AKI understanding and treatment.
Publisher
American Society for Clinical Investigation
Subject
Acute Kidney Injury - immunology
/ Acute Kidney Injury - metabolism
/ Acute Kidney Injury - pathology
/ Acute Kidney Injury - therapy
/ Animals
/ B cells
/ Epithelial Cells - immunology
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Fibrosis
/ Humans
/ Ischemia
/ Proteins
/ Review
/ Sepsis
