Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1994-8-11
pubmed:abstractText
Iron has been implicated in the pathophysiology of several models of acute and chronic renal disease. In this study, energy-dispersive x-ray spectrometry was used to quantify and localize iron in rat remnant kidneys (RK) and normal kidneys (NK) and to determine its pathophysiologic significance. Substantial iron accumulation occurred in proximal tubular cell secondary lysosomes of RK (P < 0.001 versus NK) and reached a plateau at 8 wk after partial nephrectomy. In NK, minor increases of iron also occurred with aging (P < 0.02). Proximal tubular iron accumulation correlated independently with protein excretion (r = 0.90) and impairment of GFR (r = 0.70) and was associated with tubular damage and phosphate accumulation (both P < 0.001). Iron nitrilotriacetate (1 mg/kg ip) increased tubular lysosomal iron accumulation and tubular damage (P < 0.001 versus nitrilotriacetate) in NK, comparable to levels seen in untreated RK, and increased cortical cytosolic malondialdehyde, consistent with reactive oxygen species generation. The iron chelator deferoxamine (30 mg/kg per day ip) significantly reduced iron accumulation and tubular damage in RK at 4 wk, compared with deferoxamine chelated to iron and untreated RK. These results suggest that filtered iron enters the remnant tubular lysosomes across the brush border membrane by endocytosis and may produce tubular damage in chronic renal disease by the generation of reactive oxygen species.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1598-607
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8025233-Animals, pubmed-meshheading:8025233-Creatinine, pubmed-meshheading:8025233-Deferoxamine, pubmed-meshheading:8025233-Disease Models, Animal, pubmed-meshheading:8025233-Electron Probe Microanalysis, pubmed-meshheading:8025233-Ferric Compounds, pubmed-meshheading:8025233-Infarction, pubmed-meshheading:8025233-Iron, pubmed-meshheading:8025233-Kidney, pubmed-meshheading:8025233-Kidney Failure, Chronic, pubmed-meshheading:8025233-Kidney Tubules, Proximal, pubmed-meshheading:8025233-Lysosomes, pubmed-meshheading:8025233-Male, pubmed-meshheading:8025233-Microscopy, Electron, pubmed-meshheading:8025233-Nephrectomy, pubmed-meshheading:8025233-Nitrilotriacetic Acid, pubmed-meshheading:8025233-Proteinuria, pubmed-meshheading:8025233-Rats, pubmed-meshheading:8025233-Rats, Wistar, pubmed-meshheading:8025233-Reactive Oxygen Species, pubmed-meshheading:8025233-Transferrin
pubmed:year
1994
pubmed:articleTitle
The role of tubular iron accumulation in the remnant kidney.
pubmed:affiliation
Department of Renal Medicine, Westmead Hospital, Sydney, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't