Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9405
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dc.contributor.authorHoulihan, Christine Aen
dc.contributor.authorAkdeniz, Ayselen
dc.contributor.authorTsalamandris, Conen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorJerums, Georgeen
dc.contributor.authorGilbert, Richard Een
dc.date.accessioned2015-05-15T22:29:19Z
dc.date.available2015-05-15T22:29:19Z
dc.date.issued2002-06-01en
dc.identifier.citationDiabetes Care; 25(6): 1072-7en
dc.identifier.govdoc12032117en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9405en
dc.description.abstractTransforming growth factor-beta (TGF-beta) is a prosclerotic growth factor implicated in the pathogenesis of diabetic nephropathy. In addition to high glucose, other factors implicated in renal fibrosis and increased TGF-beta synthesis include angiotensin II and high dietary sodium intake. The aim of this study was to examine the effect of angiotensin receptor blockade (ARB) and dietary sodium restriction on the plasma concentration and urinary excretion of TGF-beta in hypertensive patients with type 2 diabetes and elevated albumin excretion rate (AER).Twenty-one subjects with hypertension and AER between 10 and 200 microg/min were randomized to receive either 50 mg losartan daily (n = 11) or placebo (n = 10). Drug therapy was given in two 4-week phases, separated by a 4-week washout period. In the last 2 weeks of each phase, patients were assigned to regular- or low-sodium diets in random order. Parameters measured at week 0 and 4 of each phase included plasma TGF-beta concentration, TGF-beta urinary excretion, AER, clinic mean arterial blood pressure, and urinary sodium excretion.Plasma TGF-beta was unaffected by losartan treatment or sodium intake. In the losartan group, urinary TGF-beta excretion decreased by 23.2% (-39.2 and 13.6) [median (interquartile range)] and 38.5% (-46.8 and -6.1) in the regular- and low-sodium phases, respectively (P < 0.05 for drug effect). In the placebo group, median changes of 0.0% (-12.1 and 44.4) and 0.0% (-29.2 and 110.7) occurred in the regular- and low-sodium phases, respectively. Sodium restriction did not affect urinary TGF-beta excretion in either losartan- or placebo-treated patients (P = 0.54 for overall dietary effect), and there was no evidence of interaction between drug and diet (P = 0.29).In hypertensive type 2 diabetic patients with elevated AER, the ARB losartan, but not sodium restriction, reduced urinary TGF-beta excretion. These data suggest that the renoprotective effects of losartan in patients with type 2 diabetes and nephropathy may include a reduction in renal TGF-beta production.en
dc.language.isoenen
dc.subject.otherAlbuminuriaen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAntihypertensive Agents.therapeutic useen
dc.subject.otherBlood Pressureen
dc.subject.otherBody Mass Indexen
dc.subject.otherDiabetes Mellitus, Type 2.blood.physiopathology.urineen
dc.subject.otherDiabetic Angiopathies.urineen
dc.subject.otherDiet, Sodium-Restricteden
dc.subject.otherFemaleen
dc.subject.otherHemoglobin A, Glycosylated.analysisen
dc.subject.otherHumansen
dc.subject.otherHypertension.blood.urineen
dc.subject.otherLosartan.therapeutic useen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherPlacebosen
dc.subject.otherRegression Analysisen
dc.subject.otherSodium.urineen
dc.subject.otherTransforming Growth Factor beta.urineen
dc.titleUrinary transforming growth factor-beta excretion in patients with hypertension, type 2 diabetes, and elevated albumin excretion rate: effects of angiotensin receptor blockade and sodium restriction.en
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetes Careen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine at Austin, Victoria, Australiaen
dc.description.pages1072-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/12032117en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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