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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Nat Rev Nephrol. 2015 Feb 3;11(5):264–276. doi: 10.1038/nrneph.2015.3

Figure 2.

Figure 2

The evolution of tissue injury, death and subsequent adaptive repair after AKI. Following an episode of AKI, the kidney is capable of repair back to normal or near-normal structure and function despite apparently severe damage. Initial injury is characterized by endothelial activation, recruitment of myeloid leucocytes and widespread tubular cell injury and death. In ‘adaptive’ repair, over a period of days, debris is cleared by tubular cells and recruited macrophages, and epithelial dedifferentiation occurs followed by proliferation to restore the integrity of the tubular epithelial cell layer. Macrophages support renal growth and recovery by adopting an M2 phenotype before leaving the kidney. Pericytes remain in contact with the capillary network and do not give rise to new myofibroblasts or if they do, this myofibroblast proliferation is reversible. Abbreviations: AKI, acute kidney injury; NO, nitric oxide.