Use Of Uric Acid-lowering Agents Limits Experimental Cyclosporine Nephropathy.

dc.creatorMazali, Fernanda Cristina
dc.creatorJohnson, Richard J
dc.creatorMazzali, Marilda
dc.date2012
dc.date2015-11-27T13:29:14Z
dc.date2015-11-27T13:29:14Z
dc.date.accessioned2018-03-29T01:16:48Z
dc.date.available2018-03-29T01:16:48Z
dc.identifierNephron. Experimental Nephrology. v. 120, n. 1, p. e12-9, 2012.
dc.identifier1660-2129
dc.identifier10.1159/000330274
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/22126908
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/200377
dc.identifier22126908
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1300610
dc.descriptionHyperuricemia frequently complicates cyclosporine (CsA) therapy. Previous studies have shown that hyperuricemia exacerbates interstitial and vascular lesions in the cyclosporine model. We tested the hypothesis that normalization of uric acid could prevent the development of cyclosporine toxicity. CsA nephropathy was induced by administering CsA (15 mg/kg/day) for 7 weeks to rats on a low salt diet (CsA group). The effect of preventing hyperuricemia was determined by concomitant treatment with a xanthine oxidase inhibitor, allopurinol (CsAALP), or with a uricosuric, benzbromarone (CsABENZ), in drinking water. Control groups included vehicle-treated rats. CsA-treated rats developed mild hyperuricemia with arteriolar hyalinosis, tubular atrophy, striped interstitial fibrosis, increased cell proliferation and decreased VEGF expression. Treatment with allopurinol or benzbromarone limited renal disease, with reduced interstitial fibrosis, cell proliferation, macrophage infiltration, osteopontin expression and arteriolar hyalinosis, in association with restoration of VEGF expression. Both drugs provided comparable protection. An increase in uric acid exacerbates CsA nephropathy in the rat. Concomitant treatment with allopurinol or benzbromarone reduced the severity of renal disease. The similar protection observed with both drugs suggests that the effect is associated more with lowering uric acid levels than the antioxidant effect of allopurinol.
dc.description120
dc.descriptione12-9
dc.languageeng
dc.relationNephron. Experimental Nephrology
dc.relationNephron Exp. Nephrol.
dc.rightsfechado
dc.rightsCopyright © 2011 S. Karger AG, Basel.
dc.sourcePubMed
dc.subjectAllopurinol
dc.subjectAnimals
dc.subjectBenzbromarone
dc.subjectCell Proliferation
dc.subjectCyclosporine
dc.subjectEnzyme Inhibitors
dc.subjectFibrosis
dc.subjectHyperuricemia
dc.subjectImmunohistochemistry
dc.subjectKidney
dc.subjectKidney Diseases
dc.subjectMale
dc.subjectOsteopontin
dc.subjectRandom Allocation
dc.subjectRats
dc.subjectRats, Sprague-dawley
dc.subjectUric Acid
dc.subjectUricosuric Agents
dc.subjectVascular Endothelial Growth Factor A
dc.subjectXanthine Oxidase
dc.titleUse Of Uric Acid-lowering Agents Limits Experimental Cyclosporine Nephropathy.
dc.typeArtículos de revistas


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