Renal tubular acidosis in primary Sjogren's syndrome

dc.contributor.authorSiamopoulos, K. C.en
dc.contributor.authorElisaf, M. S.en
dc.contributor.authorDrosos, A. A.en
dc.contributor.authorMavridis, A. A.en
dc.contributor.authorMoutsopoulos, H. M.en
dc.date.accessioned2015-11-24T18:54:18Z
dc.date.available2015-11-24T18:54:18Z
dc.identifier.issn0770-3198-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18668
dc.rightsDefault Licence-
dc.subjectAcidosis, Renal Tubular/*etiologyen
dc.subjectAdulten
dc.subjectAgeden
dc.subjectAntibodies, Antinuclear/blooden
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectMiddle Ageden
dc.subjectSjogren's Syndrome/blood/*complicationsen
dc.titleRenal tubular acidosis in primary Sjogren's syndromeen
heal.abstractRenal tubular acidosis (RTA) is a frequent extraglandular manifestation of Sjogren's syndrome; however, no distinction on the incidence of this renal tubular defect between primary and secondary Sjogren's syndrome has been reported. This study was undertaken in order to define the frequency of RTA and the possible pathogenetic mechanisms in a group of 21 randomly selected primary Sjogren's syndrome patients. RTA was found in 7 (33%) patients. The incomplete type of the disorder was the most frequent. It seems that the etiology of RTA is multifactorial. Renal excretion of monoclonal proteins and the immunologically-induced interstitial inflammation are the main possible factors of this renal tubular defect.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/1617898-
heal.identifier.secondaryhttp://www.springerlink.com/content/y0653r918414l657/fulltext.pdf-
heal.journalNameClin Rheumatolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate1992-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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