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

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...

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Published in:American journal of physiology. Renal physiology 2007-10, Vol.293 (4), p.F1342-F1354
Main Authors: Han, Ki-Hwan, Kim, Hye-Young, Croker, Byron P, Reungjui, Sirirat, Lee, Su-Youn, Kim, Jin, Handlogten, Mary E, Adin, Christopher A, Weiner, I David
Format: Article
Language:English
Subjects:
Acidity
Ammonia
Ammonia - metabolism
Animals
Apoptosis
Apoptosis - physiology
Cells
Glomerular Filtration Rate - physiology
Kidney - metabolism
Kidney - pathology
Kidney - physiopathology
Kidney Tubules, Collecting - metabolism
Kidney Tubules, Collecting - pathology
Kidney Tubules, Collecting - physiopathology
Kidney Tubules, Proximal - metabolism
Kidney Tubules, Proximal - pathology
Kidney Tubules, Proximal - physiopathology
Kidneys
Loop of Henle - metabolism
Loop of Henle - pathology
Loop of Henle - physiopathology
Male
Metabolism
Models, Animal
Necrosis - physiopathology
Rats
Rats, Sprague-Dawley
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Rodents
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Summary: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.
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.00437.2006