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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1 Pt 2
|
| pubmed:dateCreated |
1989-2-23
|
| pubmed:abstractText |
To elucidate the mechanisms by which indomethacin lowers proteinuria, we studied 20 patients with the nephrotic syndrome. We performed differential macromolecule clearances before and after 3 days of therapy (150 mg/24 h). The fractional clearances of albumin and immunoglobulin G (IgG) decreased by 42 +/- 7 and 44 +/- 10%, respectively (P less than 0.05). Separation of IgG into fractions by preparative electrofocusing in eight selected individuals revealed a proportionate reduction of fractional clearances among anionic (pI = 5.0), neutral (pI = 7.5), and cationic species (pI = 8.5) of IgG. Indomethacin elevated the fractional clearance of uncharged dextrans of radius 28-44 A, while depressing those of dextrans of radius 50-60 A. A heteroporous model that depicts the major portion of the glomerular capillary wall as an isoporous membrane (pore radius = 56 A) and the minor portion as a nondiscriminatory shunt, revealed the former to be unchanged and the latter to be less prominent following indomethacin. A lower fraction of total filtrate volume permeating the shunt, together with a concomitant lowering of overall glomerular filtration rate by 24%, reduced the absolute rate of flux of macromolecule-rich fluid through the shunt pathway from 0.40 to 0.25 ml.min-1.73(-2) (P less than 0.01). We conclude that indomethacin lowered the filtered protein load by restoring barrier size-selectivity while reducing the rate of glomerular ultrafiltration.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0002-9513
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
256
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
F44-51
|
| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading |
pubmed-meshheading:2463770-Adolescent,
pubmed-meshheading:2463770-Adult,
pubmed-meshheading:2463770-Dextrans,
pubmed-meshheading:2463770-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:2463770-Female,
pubmed-meshheading:2463770-Glomerular Filtration Rate,
pubmed-meshheading:2463770-Humans,
pubmed-meshheading:2463770-Indomethacin,
pubmed-meshheading:2463770-Isoelectric Focusing,
pubmed-meshheading:2463770-Isoelectric Point,
pubmed-meshheading:2463770-Male,
pubmed-meshheading:2463770-Middle Aged,
pubmed-meshheading:2463770-Nephrotic Syndrome,
pubmed-meshheading:2463770-Proteinuria
|
| pubmed:year |
1989
|
| pubmed:articleTitle |
Mechanism of the antiproteinuric effect of indomethacin in nephrotic humans.
|
| pubmed:affiliation |
Department of Medicine, Stanford University Medical Center, California 94305.
|
| pubmed:publicationType |
Journal Article
|