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HERO ID
6728825
Reference Type
Journal Article
Subtype
Review
Title
Pathophysiology of cisplatin-induced acute kidney injury
Author(s)
Ozkok, A; Edelstein, CL
Year
2014
Is Peer Reviewed?
Yes
Journal
BioMed Research International
ISSN:
2314-6141
Volume
2014
Page Numbers
967826
Language
English
PMID
25165721
DOI
10.1155/2014/967826
Web of Science Id
WOS:000340394300001
Abstract
Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is predominantly acute tubular necrosis and also apoptosis in the proximal tubules. There is activation of multiple proinflammatory cytokines and infiltration of inflammatory cells in the kidney. Inhibition of the proinflammatory cytokines TNF-α or IL-33 or depletion of CD4+ T cells or mast cells protects against cisplatin-induced AKI. Cisplatin also causes endothelial cell injury. An understanding of the pathogenesis of cisplatin-induced AKI is important for the development of adjunctive therapies to prevent AKI, to lessen the need for dose decrease or drug withdrawal, and to lessen patient morbidity and mortality.
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