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Chronic Reduction in Renal Mass in the Rat Attenuates Ischemia/Reperfusion Injury and Does Not Impair Tubular Regeneration

SVEN R. VERCAUTEREN^*,, DIRK K. YSEBAERT, KATHLEEN E. DE GREEF^*,, ERIK J. EYSKENS and MARC E. DE BROE^*

^* Department of Nephrology-Hypertension University of Antwerp, Belgium
Department of Experimental Surgery, University of Antwerp, Belgium

Correspondence to Dr. Marc E. De Broe, Department of Nephrology- Hypertension, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium. Phone: +32 3 821 34 21; Fax: +32 3 829 01 00; E-mail: snelders{at}uia.ua.ac.be

Abstract. It is not known whether a kidney with chronic structural and functional changes is more vulnerable to an acute renal insult, and whether its regeneration capacity after injury is altered. To study this question, Lewis rats were submitted 10 wk after 5/6 nephrectomy to an ischemic insult of 60 min (remnant kidney [RK] group). Functional and morphologic data of the RK group were compared with data obtained in 10-wk uninephrectomized (1K) and normal (2K) Lewis rats with unilateral and bilateral renal ischemia, respectively. The acute postischemic decrease in creatinine clearance was smallest in the RK group, followed by the 2K and 1K groups, respectively. At days 1 and 3, fewer proximal tubules in the outer stripe of the outer medulla of the RK and 2K groups had undergone acute tubular necrosis compared with the 1K group. The mean percentage of tubules with signs of regeneration was maximal at day 3 in the three experimental groups. At day 10, regeneration was almost complete in the three groups. The number of leukocytes (OX1⁺ cells) present in the RK before ischemia did not increase after ischemia/reperfusion injury (377 ± 146 cells/mm² at day 0) in contrast to the 1K and 2K groups. In the latter groups, the number of leukocytes had increased gradually, reaching a maximum at day 15 (1K: 960 ± 308 cells/mm²) and day 10 (2K: 668 ± 164 cells/mm²), respectively. In conclusion, this study has shown that an RK exhibiting chronic morphologic changes of interstitial fibrosis and tubular atrophy is protected against ischemia/reperfusion injury, and that its regeneration capacity is preserved. The reperfusion injury is not followed by further accumulation of leukocytes, which were already present in the RK before ischemia.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673