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Abstract
Acute kidney injury (AKI) is a common clinical state resulting from pathogenic conditions
such as ischemic and toxic insults. The pathophysiology of AKI shares common pathogenic
denominators including cell death/injury, inflammation, and fibrosis, regardless of
the initiating insults. Recent clinical studies have shown that a single episode of
AKI can lead to subsequent chronic kidney disease (CKD). Although the involvement
of multiple types of cells in the pathophysiology of AKI is becoming increasingly
clear, the precise mechanisms for this "AKI to CKD progression" are still unknown,
and no drug has been shown to halt this progression. An increasing number of epidemiological
studies have also revealed that the presence of aging greatly increases the risk of
AKI to CKD progression, and chronic inflammation is increasingly recognized as an
important determinant factor for this progression. In this review article, we first
describe the current understanding of the pathophysiology of AKI to CKD progression
based on multiple types of cells. In particular, we will highlight the recent findings
in regard to the mechanisms for chronic inflammation after AKI. Subsequently, we will
focus on the mechanisms responsible for the increased risk of AKI to CKD progression
in the elderly. Finally, we highlight our recent finding of age-dependent tertiary
lymphoid tissue formation and its roles in AKI to CKD progression and speculate on
the potential therapeutic opportunities that come from targeting aberrant inflammation
after AKI.