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dc.contributor.authorJefferies, Helen
dc.contributor.authorMcIntyre, Christopher
dc.date.accessioned2016-12-01T10:10:39Z
dc.date.available2016-12-01T10:10:39Z
dc.date.issued2016-11
dc.identifier.citationHemodial Int. 2016 Nov 20. doi: 10.1111/hdi.12514.language
dc.identifier.urihttps://orda.derbyhospitals.nhs.uk/handle/123456789/765
dc.description12 Month Embargo Author(s) Pre Print Version Onlylanguage
dc.description.abstractIntroduction Repetitive dialysis-induced cardiac injury is associated with elevated troponin levels, inflammation, and longitudinal reduction in cardiac function. Pathogenic autoantibodies to cardiac troponins (cTnAAb) produce inflammatory cardiomyopathy in murine models. This study aimed to explore the possibility that analogous autoimmune processes might occur in hemodialysis (HD) patients, by initially investigating cTnAAb prevalence, and exploring potential links with HD-induced myocardial stunning. Methods In 130 prevalent HD patients from two centers (Derby, UK; Turku, Finland), cTnAAb (immunoassay) and cardiac troponins were quantified. Sixty-four patients underwent serial echocardiography to assess myocardial stunning. Findings cTnAAb were present in 7% of patients. Dual positivity to cTnAAb and elevated cTn occurred in 3% and 6% for cTnI and cTnT, respectively. Patients with cTnAAb had significantly longer dialysis vintage (82 vs. 30 months, P = 0.024), higher cTnT (0.1 vs. 0.05 pg/mL, P = 0.04), cTnI (0.02 vs. 0.01 pg/mL, P = 0.029), and free PAPP-A (6.4 vs. 3.3 mIU/L, P = 0.038). Discussion This is the first description of cTnAAb in HD patients, which raises the possibility that longitudinal exposure to repetitive HD-induced cardiac injury may lead to further autoimmune-based myocardial insult.language
dc.language.isoenlanguage
dc.subjectAutoantibodieslanguage
dc.subjectHaemodialysislanguage
dc.subjectMyocardial Stunninglanguage
dc.subjectPregnancy Associated Plasma Proteinlanguage
dc.titlePotentially pathogenic circulating autoantibodies to cardiac troponin are present in hemodialysis patients.language
dc.typeArticlelanguage


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