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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/F1342    most recent 00437.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Han, K.-H. Articles by Weiner, I. D. Search for Related Content PubMed PubMed Citation Articles by Han, K.-H. Articles by Weiner, I. D.

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct

¹Department of Anatomy, Ewha Womans University, Seoul, Korea; ²Division of Nephrology, Hypertension, and Transplantation and ³Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, Florida; ⁴Pathology and Laboratory Medical Service, Gainesville Veterans Affairs Medical Center, Gainesville, Florida; ⁵Department of Anatomy and Medical Research Center for Cell Death Disease Research Center, The Catholic University of Korea, Seoul, Korea; ⁶Department of Small Animal Clinical Sciences, Veterinary Medical Teaching Hospital, University of Florida, Gainesville, Florida; and ⁷Medical Service, Gainesville Veterans Affairs Medical Center, Gainesville, Florida

Submitted 3 November 2006 ; accepted in final form 18 July 2007

Acute renal injury induces metabolic acidosis, but its specific effects on the collecting duct, the primary site for urinary ammonia secretion, the primary component of net acid excretion, are incompletely understood. We induced ischemia-reperfusion (I/R) acute renal injury in Sprague-Dawley rats by clamping the renal pedicles bilaterally for 30 min followed by reperfusion for 6 h. Control rats underwent sham surgery without renal pedicle clamping. I/R injury decreased urinary ammonia excretion significantly but did not persistently alter urine volume, Na⁺, K⁺, or bicarbonate excretion. Histological examination demonstrated cellular damage in the outer and inner medullary collecting duct, as well as in the proximal tubule and the thick ascending limb of the loop of Henle. A subset of collecting duct cells were damaged and/or detached from the basement membrane; these cells were present predominantly in the outer medulla and were less frequent in the inner medulla. Immunohistochemistry identified that the damaged/detached cells were A-type intercalated cells, not principal cells. Both TdT-mediated dUTP nick-end labeling (TUNEL) staining and transmission electron microscopic examination demonstrated apoptosis but not necrosis. However, immunoreactivity for caspase-3 was observed in the proximal tubule, but not in collecting duct intercalated cells, suggesting that mechanism(s) of collecting duct intercalated cell apoptosis differ from those operative in the proximal tubule. We conclude that I/R injury decreases renal ammonia excretion and is associated with intercalated cell-specific detachment and apoptosis in the outer and inner medullary collecting duct. These effects likely contribute to the metabolic acidosis frequently observed in acute renal injury.

acid-base; apoptosis; intercalated cell; acute tubular necrosis