Role of renal hypoxia in the progression from acute kidney injury to chronic kidney disease

Over the past 20 years, there has been an increased appreciation of the long-term sequelae of acute kidney injury (AKI) and the potential development of chronic kidney disease (CKD). Several pathophysiologic features have been proposed to mediate AKI to CKD progression including maladaptive alterations in tubular, interstitial, inflammatory, and vascular cells. These alterations likely interact to culminate in the progression to CKD. In this article we focus primarily on evidence of vascular rarefaction secondary to AKI, and the potential mechanisms by which rarefaction occurs in relation to other alterations in tubular and interstitial compartments. We further focus on the potential that rarefaction contributes to renal hypoxia. Consideration of the role of hypoxia in AKI to CKD transition focuses on experimental evidence of persistent renal hypoxia after AKI and experimental maneuvers to evaluate the influence of hypoxia, per se, in progressive disease. Finally, consideration of methods to evaluate hypoxia in patients is provided with the suggestion that noninvasive measurement of renal hypoxia may provide insight into progression in post-AKI patients