09 BPU441269.indd

Acute kidney injury (AKI) is a common clinical syndrome directly related to patient short-term and long-term morbidity and mortality. Over the last decade, the occurrence rate of AKI has been increasing, and there has also been a growing epidemic of chronic kidney diseases (CKD) and end-stage kidney disease (ESRD) linked to severe and repeated episodes of AKIs. The detection and management of AKI are currently far from satisfactory. A large proportion of AKI patients, especially those with preexisting CKD, are at an increased risk of non-resolving AKI and progressing to CKD and ESRD. Proposed pathological processes that contribute to the transition of AKI to CKD and ESRD include severity and frequency of kidney injury, alterations of tubular cell phenotype with cells predominantly in the G2/M phase, interstitial fibrosis and microvascular rarification related to loss of endothelial–pericyte interactions and pericyte dedifferentiation. Innate immune responses, especially dendritic cell responses related to inadequate adenosine receptor (2a)mediated signals, autophagic insufficiency and reninangiotensin system activation have also been implicated in the progression of AKI and transitions from AKI to CKD and Published online: January 15, 2016 Qi Qian, MD Department of Medicine, Division of Nephrology and Hypertension Mayo Clinic College of Medicine, 200 First Street SW Rochester, MN 55905 (USA) E-Mail qian.qi @ mayo.edu © 2016 S. Karger AG, Basel 0253–5068/16/0413–0144$39.50/0