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. Author manuscript; available in PMC: 2017 Jan 14.
Published in final edited form as: Annu Rev Med. 2016 Jan 14;67:293–307. doi: 10.1146/annurev-med-050214-013407

Figure 2.

Figure 2

Maladaptive repair following acute kidney injury (AKI) leads to chronic kidney disease (CKD). In response to acute injury, there is activation of cellular stress responses, cell death pathways, and the innate immune response, which in turn lead to endothelial and epithelial dysfunction. If the injury persists or is severe, maladaptive repair mechanisms promote cell and tissue malfunction. Here, inflammation and fibrosis are central to chronic disease. Profibrotic, inflammatory macrophages are recruited. Epithelial cells that arrest in G2/M release cytokines and growth factors to promote ongoing inflammation and fibrosis. Pericytes dissociate from the endothelium to further promote endothelial dysfunction, which leads to microvascular loss. In chronic disease, extracellular matrix– depositing myofibroblasts proliferate and also form from activated, proliferating pericytes. From Reference 12 with permission.