Abstract
Abnormal IgA1 O-Glycosylation in a Multi-ethnic population of IgA Nephropathy Patients in KwaZulu Natal, South Africa.
Highlights
The pathogenesis of IgA Nephropathy (IgAN) is poorly understood globally and curative therapy currently does not exist
Novak et al reported that enhanced mesangial cell proliferation was caused by galactose-deficient IgA1-containing circulating immune complexes from the sera of IgAN patients than uncomplexed IgA1 or immune complexes from healthy control subjects (2005)
Studies in Caucasian, Asian and African American patients demonstrated elevated levels of galactose-deficient IgA1 in both IgAN patients and their first degree relatives in comparison to controls (Hastings et al, 2010; Lin et al, 2009; Gharavi et al, 2008), an additional requirement for the pathogenic mesangial deposition of IgA1 is the presence of autoantibodies specific for galactose-deficient IgA1
Summary
1.8.4 The Pathogenesis of IgAN is Incompletely Understood 1.9 Study Aim and Hypothesis CHAPTER 2 - METHODS 2.1 Concise Study Design 2.2 Ethical and Study Approval 2.3 Participant Recruitment. 2.3.1 IgAN Patient Participants 2.3.2 Control Participants and Urinalysis 2.4 Participant Description 2.4.1 Control Population Description 2.4.2 Experimental Population Description 2.5 Whole Blood Extraction and Separation 2.5.1 Whole Blood Extraction 2.5.2 Whole Blood Separation. 2.5.2.1 Sample Encoding 2.5.2.2 Whole Blood Separation and Serum Storage 2.6 IgA1 O-Glycosylation Analysis 2.6.1 Experimental Design 2.6.2 Reagent Preparation and Storage
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