Acute Kidney Injury to Chronic Kidney Disease Transition

Abstract

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.