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Abstract
Over the last 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 pathophysiological features have been proposed to mediate the
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
the role of hypoxia in the AKI to CKD transition focuses on experimental evidence
of persistent renal hypoxia following 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 non-invasive
measurement of renal hypoxia may provide insight into progression in post AKI patients.