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Cited by 417

The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.

Inflammation in Acute Kidney Injury

Open access
Kinsey, Gilbert R., Li, Li, Okusa, Mark D.·2008·Nephron Experimental Nephrology

Abstract

Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI) and evidence supporting the involvement of both innate and adaptive immunity in renal IRI has accumulated in recent years. In addition to leukocytes, kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability. Kidney tubular epithelial cells increase complement binding and upregulate toll-like receptors, both of which lead to cytokine/chemokine production in IRI. Activation of kidney resident dendritic cells, interferon-γ-producing neutrophils, infiltrating macrophages, CD4+ T cells, B cells and invariant natural killer T cells are all implicated in the pathogenesis of AKI. The complex interplay between innate and adaptive immunity in renal IRI is still not completely understood, but major advances have been made. This review summarizes these recent advances to further our understanding of the immune mechanisms of acute kidney injury.

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Metadata

Authors
Kinsey, G. R., Li, L., & Okusa, M. D.
Venue
Nephron Experimental Nephrology
Publisher
S. Karger AG
Published
2008-09-18
Volume
109
Issue
4
Pages
e102-e107
ISSN
1660-2129 (ISSN-L)
OpenAlex
W2162724808
Cited by
417
References
23
FWCI
17.76
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Inflammation in Acute Kidney Injury. https://app.cochat.ai/papers/10.1159/000142934
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Kinsey, G. R., Li, L., & Okusa, M. D. (2008). Inflammation in Acute Kidney Injury. Nephron Experimental Nephrology. https://doi.org/10.1159/000142934

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.