The outcome of acute kidney injury (AKI) may vary from complete resolution to an incomplete recovery of renal function leading to chronic kidney disease (CKD). An increasing body of evidence suggests a causal link between AKI and the consequent development of CKD. The outcome of AKI depends, at the tissue level, on the balance of adaptive and maladaptive repair. Maladaptive repair is characterized by the development of interstitial fibrosis, persistent expression of fibrogenic factors, and delayed resolution of inflammation.Tubular and endothelial cells are the main actors in the pathogenesis of AKI and in the events leading to its resolution. However, in the last two decades we recognized the key role of other resident cells, including pericytes, in maladaptive repair. On the other hand, the activation of the innate immune system always has been considered essential in the development of renal injury and in its repair, although evidence now supports a key role also for infiltrating B and T cells in this setting. All of these changes observed in the process leading from acute to chronic tissue injury clearly suggest the acceleration of a physiologic senescence process. Thus accelerated cell and tissue senescence as the main pathogenic mechanism of maladaptive repair may represent a unifying hypothesis.
|Titolo della pubblicazione ospite||Critical Care Nephrology: Third Edition|
|Numero di pagine||5|
|Stato di pubblicazione||Pubblicato - 2019|
- Innate immunity
- Tubular cells