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, 109 (4), e102-7

Inflammation in Acute Kidney Injury


Inflammation in Acute Kidney Injury

Gilbert R Kinsey et al. Nephron Exp Nephrol.


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-gamma-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.


Fig. 1
Fig. 1
Inflammatory role of bone marrow-derived and kidney cells in AKI. Ischemia-reperfusion induces changes in leukocytes, endothelial cells and tubular epithelial cells that result in kidney inflammation and mediate AKI. Bone marrow derived cells such as iNKT cells [3], neutrophils (PMN [3, 4, 12]) and macrophages (MØ [16]) accumulate in the kidney, are activated and produce pro-inflammatory cytokines (i.e. IFN-γ production by iNKT cells and PMNs [3]). Endothelial cells are damaged by IRI leading to increased vascular permeability [8, 9] and expression of adhesion molecules such as ICAM-1 [4] and fractalkine [10]. These changes facilitate the accumulation of leukocytes in the kidney. Renal dendritic cells produce cytokines and chemokines [17] and traffic to the renal draining lymph node and present antigens to T cells [18]. Tubular epithelial cells exhibit increased complement deposition [2] and upregulate the expression of toll-like receptors (TLRs [12, 13]), both of which mediate chemokine and cytokine production in the injured kidney [11-13]. Changes in each cell type directly or indirectly influence the other cells involved to promote inflammation after renal IRI. These interactions between kidney and bone marrow derived cells and between innate and adaptive immunity demonstrate the complex nature of the inflammation associated with AKI.

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