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1 Anatomy, Ewha Womans University, Seoul, Korea, Republic of
2 Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville, Florida, United States
3 North Florida/South Georgia Veterans Health System, Pathology and Laboratory Medicine Service and Department of Pathology, Immun, University of Florida, Gainesville, Florida, United States
4 Department of Anatomy, Ewha Womans University, Seoul, Korea, Republic of
5 Anatomy, The Catholic University of Korea, Seoul, Korea, Republic of
6 Small Animal Clinical Sciences, University of Florida, Gainesville, Florida, United States
7 Div. of Nephrol., Hypertension & Transplant., Univ. of Fla. College of Medicine, P.O. Box 100224, Gainsville, Florida, 32610, United States; Nephrology and Hypertension Section, NF/SGVHS, Gainesville, Florida, United States
* To whom correspondence should be addressed. E-mail: weineid{at}ufl.edu.
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 injury (IRI) acute renal injury in Sprague-Dawley rats by clamping the renal pedicles bilaterally for 30 minutes followed by reperfusion for 6 hours. Control rats underwent sham surgery without renal pedicle clamping. IRI decreased urinary ammonia excretion significantly, but did not persistently alter urine volume, Na+, K+ or bicarbonate excretion. Histologic 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 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 IRI 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.
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