Linked Life Data

3666586

Source:http://linkedlifedata.com/resource/pubmed/id/3666586

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1987-11-30
pubmed:abstractText
The metabolism and urinary excretion of 125I antithrombin III (AT III) was investigated in 2 patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis, and acquired deficiency of AT III. Increased AT III catabolism was observed in both patients, even after correction for urinary protein loss. Increased AT III catabolism was due to increased influx from the extra- to the intravascular compartment in 1 patient, and to an increased fractional catabolic rate in the other patient who developed later a pulmonary embolism. Analysis of urine samples revealed biologically inactive whole AT III molecules and biologically as well as antigenically inactive fragments, respectively, whereas daily plasma gel filtration showed intact radioactive AT III. These observations reject the hypothesis that AT III deficiency in nephrotic patients is only due to urinary loss of AT III.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0301-0147
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
286-92
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Antithrombin III metabolism in two patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis.
pubmed:affiliation
Department of Hematology, University of Amsterdam, The Netherlands.
pubmed:publicationType
Journal Article, Case Reports