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BACKGROUND: Haemodialysis patients are extremely vulnerable to COVID-19. Their immune response after infection is unclear. We have found high seroconversion rates in this population with 95% developing antibodies. It is unclear if and how long these antibodies persist. Here we investigate this with serial antibody testing. METHODS: We identified haemodialysis patients who had confirmed SARS-CoV-2 between March-May 2020 and measured monthly antibodies (IgG/IgM) in those who survived. We used a semi-quantitative cut-off index (COI) to create a qualitative result and plotted optical density (OD) over time. We used linear regression to examine the slope, as well as noting peak OD and time to peak OD. We correlated these against baseline demographics, markers of illness severity, and comorbidities. RESULTS: 122 patients were analysed. All remained antibody positive during follow-up; for a minimum of 148 days. 71% had a positive gradient indicating increasing antibody positivity over time. We found that age (p = 0.01), duration of PCR positivity (p = 0.06) and presence of symptoms (p = 0.05) were associated with a longer time to peak OD. Immunosuppression did not alter peak OD but did lead to a non-significant increase in time to peak OD and more patients had a subsequent fall in Ab levels (p = 0.02). Diabetic patients were more likely to have a positive slope (OR 2.26). CONCLUSIONS: These results indicate that haemodialysis patients have a robust and sustained antibody response after confirmed COVID-19 infection with no suggestion that immunosuppression weakens this response. Although unclear what protection these antibodies confer, this encouraging that haemodialysis patients should respond to vaccination.
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INTRODUCTION: IgG anti-apolipoprotein A-1 (IgG anti-apoA-1) antibodies are present in patients with systemic lupus erythematosus (SLE) and may link inflammatory disease activity and the increased risk of developing atherosclerosis and cardiovascular disease (CVD) in these patients. We carried out a rigorous analysis of the associations between IgG anti-apoA-1 levels and disease activity, drug therapy, serology, damage, mortality and CVD events in a large British SLE cohort. METHODS: Serum IgG anti-apoA-1 levels were measured in 100 healthy controls to define a cut-off for positivity. In 499 patients with SLE we obtained the earliest stored serum sample from their disease course and measured IgG anti-apoA-1 level. We then examined associations between IgG anti-apoA-1 positivity in early disease and the development of damage, CVD or death over a mean follow-up period of 12.1 years in these patients. In a separate study, we measured IgG anti-apoA-1 levels in 397 samples taken longitudinally from 49 patients with SLE over a mean period of 89 months of fluctuating disease activity and carried out multi-variable analysis to examine the demographic, serological, disease activity and treatment factors associated with IgG anti-apoA-1 level over time. RESULTS: In the longitudinal study, IgG anti-apoA-1 levels were significantly higher in patients with persistently active disease, those on high dose corticosteroid and those not taking hydroxychloroquine. Of the 499 subjects who had early disease IgG anti-apoA-1 levels measured, 135 (27%) were positive. However, we found no convincing associations between early IgG anti-apoA-1 positivity and development of damage, mortality or CVD. CONCLUSIONS: IgG anti-apoA-1 developed early in a quarter of our patients with SLE, but this had no major impact on subsequent clinical outcomes. However, levels of IgG anti-apoA-1 vary over time and are associated with disease activity, treatment with high dose corticosteroid and not taking hydroxychloroquine.
