Reprint

Kidney Inflammation, Injury and Regeneration 2020

Edited by
November 2021
318 pages
  • ISBN978-3-0365-2370-5 (Hardback)
  • ISBN978-3-0365-2369-9 (PDF)

This book is a reprint of the Special Issue Kidney Inflammation, Injury and Regeneration 2020 that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of chronic kidney disease in the sequel. Whereas the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function—in both the short- and long-term—is urgently needed. This Special Issue includes papers investigating the pathological mechanisms of renal inflammation and AKI and diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to attenuate kidney dysfunction are included, as well as review articles.

Format
  • Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
inflammation; chronic kidney disease; anemia; anemia of inflammation; ESA hyporesponsiveness; renal tubular epithelial cells; macrophages; lipocalin-2; iron; cilastatin; hypoxia inducible factor-1-α; ischemia-reperfusion injury; acute kidney injury; chronic kidney disease; cyclophilin A; fibrosis; inflammation; renal fibrosis; tubular necrosis; preeclampsia; podocytes; VEGF; FSGS; proteinuria; endocan; ESM-1; acute kidney injury; chronic kidney disease; renal replacement therapy; kidney transplantation; acute kidney injury; biomarker; diabetic nephropathy; focal segmental glomerulosclerosis; innate immunity; membranous nephropathy; minimal change diseases; TLR; NOX1; ML171; reactive oxygen species; ERK; ischemia-reperfusion injury; acute kidney injury; inflammation; T cells; glomerulonephritis; innate immunity; chemokines; renal disease; DJ-1; ND-13; renal inflammation; oxidative stress; UUO; fibrosis; ischemia-reperfusion injury; acute kidney injury; autophagy; apoptosis; trehalose; simvastatin; endotoxin; tubular apoptosis; cytochrome C; Bcl-XL; survivin; chronic kidney disease; hypercholesterolemia; xanthine oxidase; inflammation; fibrosis; NF-κB pathway; tertiary lymphoid organs; kidney transplantation; B cells; BAFF; kidney fibrosis; inflammation; myofibroblast activation; extracellular matrix; Hippo pathway; verteporfin; IgAN; proteinuria; CKD; progression; ACEI; corticosteroids; costimulation; coinhibition; ischemia-reperfusion injury; kidney transplant; SPR; protein binding affinity; innate immunity; adaptive immunity; inflammation; epithelial-to-mesenchymal transition; E. cava extracts; dieckol; spontaneously hypertensive rats; renal fibrosis; angiotensin II; n/a