Linked Life Data

9848785

Source:http://linkedlifedata.com/resource/pubmed/id/9848785

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1999-4-19
pubmed:abstractText
Evidence is available from animal and human studies that protein traffic through the glomerular capillary has a pathogenetic role in subsequent renal damage and that angiotensin-converting enzyme (ACE) inhibitors appear superior to other drugs in lowering proteinuria and the rate of renal function decline. This study compares the effect of ACE inhibition or angiotensin II (AngII) receptor blockade on urinary protein excretion and renal hemodynamics in 20 patients with IgA glomerulonephritis randomized to receive enalapril (20 mg/d) or irbesartan (100 mg/d) for 28 d in a double-blind study with two parallel groups. This study also evaluated whether addition of indomethacin (75 mg twice a day) to each of the two treatments resulted in a more potent antiproteinuric effect. Enalapril alone reduced total protein excretion (61% change from baseline) and fractional clearance of albumin without changes in GFR and minor elevation in renal plasma flow. Also, patients randomized to receive the AngII receptor antagonist irbesartan for 28 d had lower proteinuria (55% change from baseline) and fractional clearance of albumin at the end of the treatment period with similar renal hemodynamic changes. When indomethacin was added to enalapril treatment, a further significant reduction in urinary proteins and fractional albumin clearance was observed. In patients given irbesartan, the addition of indomethacin further reduced proteinuria and fractional clearance of albumin. The combined therapy with enalapril or irbesartan and indomethacin did not significantly affect GFR and renal plasma flow compared with baseline. These findings indicate that in patients with IgA glomerulonephritis the antiproteinuric effect of blocking AngII activity by either ACE inhibitors or AngII receptor antagonists is potentiated by indomethacin, an effect that occurred without impairment of renal function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2308-17
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9848785-Adult, pubmed-meshheading:9848785-Aged, pubmed-meshheading:9848785-Angiotensin Receptor Antagonists, pubmed-meshheading:9848785-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:9848785-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:9848785-Antihypertensive Agents, pubmed-meshheading:9848785-Biphenyl Compounds, pubmed-meshheading:9848785-Blood Pressure, pubmed-meshheading:9848785-Double-Blind Method, pubmed-meshheading:9848785-Drug Synergism, pubmed-meshheading:9848785-Drug Therapy, Combination, pubmed-meshheading:9848785-Enalapril, pubmed-meshheading:9848785-Female, pubmed-meshheading:9848785-Glomerulonephritis, IGA, pubmed-meshheading:9848785-Humans, pubmed-meshheading:9848785-Hypertension, Renal, pubmed-meshheading:9848785-Indomethacin, pubmed-meshheading:9848785-Kidney Function Tests, pubmed-meshheading:9848785-Male, pubmed-meshheading:9848785-Middle Aged, pubmed-meshheading:9848785-Proteinuria, pubmed-meshheading:9848785-Renal Circulation, pubmed-meshheading:9848785-Tetrazoles, pubmed-meshheading:9848785-Treatment Outcome
pubmed:year
1998
pubmed:articleTitle
The antiproteinuric effect of angiotensin antagonism in human IgA nephropathy is potentiated by indomethacin.
pubmed:affiliation
Department of Kidney Research, Mario Negri Institute for Pharmacological Research, Bergamo, Italy.
pubmed:publicationType
Journal Article, Clinical Trial, Comparative Study, Randomized Controlled Trial, Research Support, Non-U.S. Gov't