Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1995-2-8
pubmed:abstractText
Loss of renal functional reserve, that is, absence of the glomerular vasodilatory response to amino-acid infusion, has been interpreted as equivalent to glomerular hyperperfusion/hypertension, and therefore proposed as a marker of high risk for progressive glomerular sclerosis. To substantiate the validity of this hypothesis we evaluated the renal response to glycine and the extent of glomerular damage 10-12 weeks after induction of anti-glomerular basement membrane glomerulonephritis with or without superimposed clip hypertension. Untreated rats and rats chronically treated with quinapril, a converting-enzyme inhibitor, were studied. In untreated groups, loss of renal functional reserve was demonstrated since GFR, single-nephron GFR (SNGFR) and plasma flow (SNPF) did not increase during glycine infusion. The absence of renal reserve was associated with glomerular hyperfusion/hypertension, and development of proteinuria and glomerulosclerosis. Quinapril reduced proteinuria and diffuse sclerosis in anti-glomerular basement membrane GN, and decreased blood pressure and segmental glomerulosclerosis in antiglomerular basement membrane GN with superimposed clip hypertension. Both treated groups demonstrated a restoration of renal functional reserve, as depicted by increases in GFR, SNGFR, and SNPF after glycine, despite persistence of glomerular hyperperfusion/hypertension. These data demonstrate that renal functional reserve testing, although it does not detect glomerular hyperperfusion/hypertension, can provide information on the progression of glomerular damage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0931-0509
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1383-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7816249-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:7816249-Animals, pubmed-meshheading:7816249-Antibodies, pubmed-meshheading:7816249-Antihypertensive Agents, pubmed-meshheading:7816249-Basement Membrane, pubmed-meshheading:7816249-Chronic Disease, pubmed-meshheading:7816249-Glomerulonephritis, pubmed-meshheading:7816249-Glycine, pubmed-meshheading:7816249-Hypertension, Renovascular, pubmed-meshheading:7816249-Isoquinolines, pubmed-meshheading:7816249-Kidney, pubmed-meshheading:7816249-Kidney Function Tests, pubmed-meshheading:7816249-Kidney Glomerulus, pubmed-meshheading:7816249-Kidney Tubules, pubmed-meshheading:7816249-Male, pubmed-meshheading:7816249-Rats, pubmed-meshheading:7816249-Rats, Wistar, pubmed-meshheading:7816249-Renal Circulation, pubmed-meshheading:7816249-Tetrahydroisoquinolines
pubmed:year
1994
pubmed:articleTitle
Renal functional reserve in experimental chronic glomerulonephritis.
pubmed:affiliation
Division of Nephrology-Hypertension, University of California, San Diego School of Medicine.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't