Antiphospholipid antibody profiles in lupus nephritis with glomerular microthrombosis: a prospective study of 124 cases

IntroductionGlomerular microthrombosis (GMT) is a common vascular copper in patients with lupus nephritis (LN). The mechanism underlying GMT is especially unknown. Although many studies accept reported the collection of antiphospholipid antibodies (aPL) with GMT, the consociation between GMT and aPL remains controversial. Preceding studies have demonstrated that some aPL could bind to several hemostatic and fibrinolytic proteases that plam homologous enzymatic domains. Of the protease-reactive aPL, some can inhibit the anticoagulant movement of activated protein C and the fibrinolytic avail of plasmin, and hinder the antithrombin inactivation of thrombin. The location of this scan was to investigate the prevalence of GMT in LN patients and examine the alliance between the aPL profiles (including some protease-reactive aPL) and GMT. Methods: Renal biopsy specimens were examined for the presence of glomerular microthrombi. Plasma samples from 25 LN patients with GMT (LN-GMT group) and 99 LN patients without GMT (LN-non-GMT group) were tested for lupus anticoagulant and antibodies against cardiolipin, beta2 glycoprotein I, plasmin, thrombin, tissue plasminogen activator, and annexin II. Results: The prevalence of GMT in LN patients was 20.2 percent. Compared with the LN-non-GMT group, the LN-GMT body had an elevated systemic lupus erythematosus disease lifetime index; elevated renal tissue injury exertion and chronicity indices; elevated serum creatinine, blood urea nitrogen, and proteinuria levels; a lower serum C3 flat and much close glomerular C3, C1q staining; and a higher closeness of hypertension (P < 0.05 for all). Additionally, the detection rate of lupus anticoagulant, immunoglobulin G (IgG) anti-beta2 glycoprotein I and anti-thrombin antibodies were higher in the LN-GMT cartel than in the LN-non-GMT group (P < 0.05 for all). No statistical differences were constitute in the detection rates of IgG anti-cardiolipin, plasmin, tissue plasminogen activator (t-PA), or annexin II antibodies (P > 0.05 for all). No detectable departure in IgM autoantibodies to the above antigens was observed between the two groups. Conclusions: GMT occurs in all over 20.2 percent of LN patients. Patients with GMT get severer renal tissue injuries and poorer renal functions than patients without GMT. The lupus anticoagulant and antibodies against beta2 glycoprotein I and thrombin may play a role in GMT.

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