Abstract
Background and objectivesThe underlying mechanism of IgA vasculitis (IgAV) and IgA vasculitis with nephritis (IgAVN) remains unclear. Therefore, there are no accurate diagnostic methods. Lipid metabolism is related to many immune related diseases, so this study set out to explore the relationship of lipids and IgAV and IgAVN.MethodsFifty-eighth patients with IgAV and 28 healthy controls were recruited, which were divided into six separate pools to investigate the alterations of serum lipids according to the clinical characteristics: healthy controls group (HCs) and IgAV group (IgAVs), IgAVN group (IgAV-N) and IgAV without nephritis group (IgAV-C), initial IgAV group (IgAV0) and IgAV in treatment with glucocorticoids group (IgAV1).Results31 identified lipid ions significantly changed in IgAVs with p < 0.05, variable importance of the projection (VIP) > 1 and fold change (FC) > 1.5. All these 31 lipid ions belong to 6 classes: triacylglycerols (TG), phosphatidylethanolamine (PE), phosphatidylcholine (PC), phosphatidylserine, ceramide, and lysophosphatidylcholine. TG (16:0/18:1/22:6) +NH4 over 888875609.05, PC (32:1) +H over 905307459.90 and PE (21:4)-H less than 32236196.59 increased the risk of IgAV significantly (OR>1). PC (38:6) +H was significantly decreased (p < 0.05, VIP>1 and FC>1.5) in IgAVN. PC (38:6) less than 4469726623 conferred greater risks of IgAV (OR=45.833, 95%CI: 6.689~341.070).ConclusionWe suggest that lipid metabolism may affect the pathogenesis of IgAV via cardiovascular disease, insulin resistance, cell apoptosis, and inflammation. The increase of TG(16:0/18:1/22:6) + NH4, and PC(32:1) + H as well as PE (21:4)-H allow a good prediction of IgAV. PE-to-PC conversion may participate in the damage of kidney in IgAV. PC (38:6) + H may be a potential biomarker for IgAVN.
Highlights
IgA vasculitis (IgAV), referred to as HenochSchönlein purpura (HSP), is the most common systemic vasculitis in children with an annual incidence of 3 ~ 26.7 cases per 100,000 [1]
Most researchers believe IgAV is related to the high level of IgA1-AECA, which binds to small vessels to induce cytokines that recruit neutrophils activated by the interaction between IgA1 and its receptor FcαRI, resulting in inflammation [3]
Most methods for diagnosis and treatment of IgA vasculitis with nephritis (IgAVN) are based on studies of IgA nephropathy, which is closely related with galactosedeficient IgA1 [10, 11]
Summary
IgA vasculitis (IgAV), referred to as HenochSchönlein purpura (HSP), is the most common systemic vasculitis in children with an annual incidence of 3 ~ 26.7 cases per 100,000 [1]. Most methods for diagnosis and treatment of IgAVN are based on studies of IgA nephropathy, which is closely related with galactosedeficient IgA1 [10, 11]. The mechanism of IgAV and IgAVN required further investigation to define potential biomarkers to assist in the early detection and accurate diagnosis for improving the prognosis of IgAV. The underlying mechanism of IgA vasculitis (IgAV) and IgA vasculitis with nephritis (IgAVN) remains unclear. Lipid metabolism is related to many immune related diseases, so this study set out to explore the relationship of lipids and IgAV and IgAVN
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