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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-5-21
pubmed:abstractText
Chronic hypoxia likely plays a pivotal role in chronic renal disease, but the specifics of its involvement remain unclear. To elucidate how chronic hypoxia occurs and whether hypoxia participates in the progression of renal disease, the authors established an irreversible glomerulonephritis model induced by uninephrectomy and repeated anti-Thy-1 antibody injections. Glomerulosclerosis with microvascular obliteration was complete at 2 wk after antibody injection and was not restored until 11 wk. Tubulointerstitial injury was mild at 2 wk and was gradually exacerbated until 11 wk, a pattern that was in accordance with the loss of peritubular capillaries. Immunohistochemical analysis using pimonidazole revealed the augmentation of hypoxia in the cortex before the aggravation of tubulointerstitial injury and subsequent peritubular capillary loss. The preexistence of hypoxia implies that it had substantial participation in the progression of tubulointerstitial injury. To test whether blood flow was inhibited in diseased kidneys, capillaries with intact blood flow were identified by tail vein injection of biotinylated lectin specific to endothelial cells. The renal microvasculature was well recognized by lectin in the controls, whereas lectin binding to peritubular capillaries was strikingly decreased in diseased kidneys, suggesting a disturbance of blood flow. Intravital microscopy analysis confirmed that blood flow in peritubular capillaries was decreased by approximately 40% in the disease group compared with the controls. In conclusion, stagnation of blood flow in peritubular capillaries induced chronic hypoxia at an early stage in this model, which was followed by progressive tubulointerstitial injury and a loss of peritubular capillaries.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1574-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15153568-Animals, pubmed-meshheading:15153568-Anoxia, pubmed-meshheading:15153568-Biotinylation, pubmed-meshheading:15153568-Blood Urea Nitrogen, pubmed-meshheading:15153568-Capillaries, pubmed-meshheading:15153568-Disease Progression, pubmed-meshheading:15153568-Endothelial Cells, pubmed-meshheading:15153568-Glomerulonephritis, pubmed-meshheading:15153568-Immunohistochemistry, pubmed-meshheading:15153568-Kidney, pubmed-meshheading:15153568-Lectins, pubmed-meshheading:15153568-Male, pubmed-meshheading:15153568-Microscopy, pubmed-meshheading:15153568-Nephritis, pubmed-meshheading:15153568-Nephritis, Interstitial, pubmed-meshheading:15153568-Perfusion, pubmed-meshheading:15153568-Rats, pubmed-meshheading:15153568-Rats, Sprague-Dawley, pubmed-meshheading:15153568-Time Factors
pubmed:year
2004
pubmed:articleTitle
Hypoperfusion of peritubular capillaries induces chronic hypoxia before progression of tubulointerstitial injury in a progressive model of rat glomerulonephritis.
pubmed:affiliation
Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't