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

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Abstract Text:

Ki-Hwan Han,Hye-Young Kim,Byron P Croker,Sirirat Reungjui,Su-Youn Lee,Jin Kim,Mary E Handlogten,Christopher A Adin,I David Weiner,

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.

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Publishing Authors By Initials

KH Han,HY Kim,BP Croker,S Reungjui,SY Lee,J Kim,ME Handlogten,CA Adin,ID Weiner,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Renal physiology

VOLUME: 293

Page Numbers: F1342-54

Journal Abbreviation: Am. J. Physiol. Renal Physiol.

ISSN: 0363-6127

DAY: 8

MONTH: 08

YEAR: 2007

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

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901990

Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Effects of ischemia-reperfusion injury on renal ammonia metabolism and the collecting duct.

AFFILIATION: Department of Anatomy, Ewha Womans University, Seoul, Korea.

Country: United States

AGENCY: United States NINDS

GRANT: NS-47624

ACRONYM: NS

MEDLINETA: Am J Physiol Renal Physiol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

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

• A randomized clinical trial comparing the effect of maternal intravenous hydration and placebo on the amniotic fluid index in oligohydramnios.
• ADCS Prevention Instrument Project: quality of life assessment (QOL).
• Adapting a dynamic model of interorganizational cooperation to the health care sector.
• Anisotropic Poisson's ratio and compression modulus of cortical bone determined by speckle interferometry.
• Bayesian parallel imaging with edge-preserving priors.
• Binding of mitochondrial leader sequences to Tom20 assessed using a bacterial two-hybrid system shows that hydrophobic interactions are essential and that some mutated leaders that do not bind Tom20 can still be imported.
• Biomechanical properties of the lower uterine segment above and below the reflection of the urinary bladder flap.
• Cardiovascular disease and subsequent kidney disease.
• Caregiving burden responses differ for Internet and telephone data collection.
• Chronic low back pain in older adults: What physicians know, what they think they know, and what they should be taught.
• Cognitive dysfunction in patients with clinically isolated syndromes or newly diagnosed multiple sclerosis.
• Cutting Edge: Immature human dendritic cells express latency-associated peptide and inhibit T cell activation in a TGF-beta-dependent manner.
• Delivery of drugs and macromolecules to mitochondria.
• Different regional patterns of cortical thinning in Alzheimer's disease and frontotemporal dementia.
• Efficacy of novel plasmid DNA encoding vaccinia antigens in improving current smallpox vaccination strategy.
• Electronic health records: high-quality electronic data for higher-quality clinical research.
• Expression of the ammonia transporter, rh C glycoprotein, in normal and neoplastic human kidney.
• How the parallel channels of the retina contribute to depth processing.
• Measurement of hippocampal subfields and age-related changes with high resolution MRI at 4T.
• Plasma 24S hydroxycholesterol response to statins in Alzheimer's disease patients: effects of gender, CYP46, and ApoE polymorphisms.
• Quantitative bioanalytical methods validation and implementation: best practices for chromatographic and ligand binding assays.
• Recovery preference exploration: analysis of patient feedback after imagined scenarios.
• Reengineering CCA-adding enzymes to function as (U,G)- or dCdCdA-adding enzymes or poly(C,A) and poly(U,G) polymerases.
• Regulation of antibody-dependent cellular cytotoxicity by IgG intrinsic and apparent affinity for target antigen.
• Th3 cells in peripheral tolerance. I. Induction of Foxp3-positive regulatory T cells by Th3 cells derived from TGF-beta T cell-transgenic mice.
• Th3 cells in peripheral tolerance. II. TGF-beta-transgenic Th3 cells rescue IL-2-deficient mice from autoimmunity.
• The hairless mouse ear: an in vivo model for studying wound neovascularization.
• The quinone binding site in Escherichia coli succinate dehydrogenase is required for electron transfer to the heme b.
• Voxel-based T2 relaxation rate measurements in temporal lobe epilepsy (TLE) with and without mesial temporal sclerosis.
• X-ray absorption spectroscopic characterization of the molybdenum site of Escherichia coli dimethyl sulfoxide reductase.