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Originally published as JHC exPRESS on February 20, 2007.
doi:10.1369/jhc.6A7130.2007
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Journal of Histochemistry and Cytochemistry
Volume 55 (6): 575-584, 2007
Copyright ©The Histochemical Society, Inc.

Alteration in Renal Organic Anion Transporter 1 After Ischemia/Reperfusion in Cadaveric Renal Allografts

Osun Kwon, Seok-Min Hong and Kristina Blouch

Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana (OK,S-MH), and Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California (KB)

Correspondence and present address: Osun Kwon, MD, PhD, Penn State College of Medicine, Division of Nephrology, Department of Medicine, H040, 500 University Dr., Hershey, PA 17033-0850. E-mail: okwon{at}psu.edu

We have previously shown that postischemic injury to renal allografts results in profound impairment of p-aminohippuric acid (PAH) extraction. To elucidate the cellular integrity of the human organic anion transporter 1 (hOAT1) in postischemic acute renal failure (ARF), immunohistochemical analysis of hOAT1 was performed in cadaveric renal allografts using confocal microscopy for three-dimensional reconstruction of serial optical images. Biopsy samples were obtained from 10 cadaveric renal allografts 1 hr after reperfusion during transplant operation. Control tissues were obtained from four living donors of healthy kidneys immediately before an arterial clamp was applied to the renal artery. Control tissues demonstrated hOAT1 distributed to basolateral membrane of proximal tubule cells. In contrast, maldistribution of hOAT1 to cytoplasm and/or diminution of the protein was noted in cadaveric allografts. Characteristics of maldistribution were variable: disappearance of lateral distribution, diffuse cytoplasmic aggregates, apical cytoplasmic aggregates, and disappearance of the staining. In addition, iothalamate and PAH clearances were performed on posttransplant days 3–7 in 18 recipients of a cadaveric renal allograft. PAH clearance was depressed <250 ml/min in all but three subjects. We conclude that reperfused, transplanted kidneys exhibit maldistribution of hOAT1 in proximal tubule cells, resulting in impairment of PAH clearance. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials. (J Histochem Cytochem 55:575–584, 2007)

Key Words: postischemic acute renal failure • renal tubular secretion • human organic anion transporter 1 • confocal microscopy


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