Background: Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end-stage renal disease (ESRD). In the previous years, novel insights in the pathophysiology of CKD progression suggested a causal link between AKI and CKD due to a maladaptive repair after severe and repeated injury. Summary: Several pathological mechanisms have been proposed to contribute to the progression of AKI and transition to CKD/ESRD including hypoxia and microvascular rarefaction, alterations of renal resident cell phenotypes and functions, cell cycle arrest in the G2/M phase, persistent chronic inflammation, and development of interstitial fibrosis, mitochondrial fragmentation, epigenetic changes, activation of renin-angiotensin system (RAS), cell and tissue senescence. Furthermore, several clinical factors have been identified such as severity of AKI, age, and comorbidities. The identification of AKI-to-CKD biomarkers could improve the early identification of AKI patients with higher risk for CKD progression. However, although our understanding in the pathophysiology of AKI-to-CKD transition is significantly improved, no novel intervention has been validated. Potential therapeutic approaches to treat AKI and block the transition to CKD/ESRD have been recently reported, but they need further validations. Key Messages: Maladaptive repair after AKI is strongly associated to the development of CKD and long-term consequences. The prompt identification of patients at higher risk for late CKD progression and the development of new therapeutic interventions remain critical research goals.
Acute Kidney Injury to Chronic Kidney Disease Transition
Castellano, Giuseppe
2018-01-01
Abstract
Background: Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end-stage renal disease (ESRD). In the previous years, novel insights in the pathophysiology of CKD progression suggested a causal link between AKI and CKD due to a maladaptive repair after severe and repeated injury. Summary: Several pathological mechanisms have been proposed to contribute to the progression of AKI and transition to CKD/ESRD including hypoxia and microvascular rarefaction, alterations of renal resident cell phenotypes and functions, cell cycle arrest in the G2/M phase, persistent chronic inflammation, and development of interstitial fibrosis, mitochondrial fragmentation, epigenetic changes, activation of renin-angiotensin system (RAS), cell and tissue senescence. Furthermore, several clinical factors have been identified such as severity of AKI, age, and comorbidities. The identification of AKI-to-CKD biomarkers could improve the early identification of AKI patients with higher risk for CKD progression. However, although our understanding in the pathophysiology of AKI-to-CKD transition is significantly improved, no novel intervention has been validated. Potential therapeutic approaches to treat AKI and block the transition to CKD/ESRD have been recently reported, but they need further validations. Key Messages: Maladaptive repair after AKI is strongly associated to the development of CKD and long-term consequences. The prompt identification of patients at higher risk for late CKD progression and the development of new therapeutic interventions remain critical research goals.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.