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.