Renal solute clearances are reduced in ischemic acute kidney injury (AKI). However, the mechanisms explaining how solute clearance is impaired have not been clarified. Recently, we reported that cadaveric renal allografts exhibit maldistribution of organic anion transporter 1 (OAT1) in proximal tubule cells after ischemia and reperfusion, resulting in impairment of p-aminohippuric acid clearance. The present study characterized renal OAT1 in detail after ischemia-reperfusion, using a rat model. Renal OAT1 was analyzed using confocal microscopy with a three-dimensional reconstruction of serial optical images, Western blot, and quantitative real-time RT-PCR. OAT1 was distributed to basolateral membranes of proximal tubule cells in controls. With ischemia, OAT1 decreased in basolateral membrane, especially lateral membrane domain and appeared diffusely in cytoplasm. After reperfusion following 60 min ischemia, it often formed cytoplasmic aggregates. The staining for OAT1 started reappearing in lateral membrane distribution an hour after reperfusion. The basolateral membrane staining is relatively well discernable at 240 hours of reperfusion. Of note, distinct increase in OAT1 expression was noted in vasculature early after ischemia and following reperfusion. The total amount of OAT1 protein expression in the kidney diminished after ischemia-reperfusion in a duration-dependant manner until 72 hrs, when they began to recover. However, even at 240 hrs, the amount of OAT1 did not reach control levels. The kidney tissues tended to show a remarkable but transient increase in mRNA expression for OAT1 at 5 min ischemia. Our findings may provide insights of renal OAT1 in its cellular localization and response during ischemic AKI and recovery from it.