No Association of Homocysteine, Anticardiolipin Antibody, and Anti-ß2 Glycoprotein I Antibody With Portal Venous System Thrombosis in Liver Cirrhosis.

Portal venous system thrombosis (PVST), a common complication of liver cirrhosis, is closely associated with thrombophilia. To explore the association of homocysteine (Hcy), anticardiolipin antibody (aCL), and anti-ß2 glycoprotein I antibody (aß2GPI), which are possible thrombophilic factors, with PVST in liver cirrhosis. Overall, 654 non-malignant patients (219 with and 435 without liver cirrhosis) admitted between January 2016 and June 2020 were retrospectively evaluated. Presence of PVST, degree of main portal vein (MPV) thrombosis, and clinically significant PVST were identified. Hcy level, hyperhomocysteinemia (HHcy), aCL positivity, and aß2GPI positivity were compared according to the presence of liver cirrhosis and PVST. Positive aß2GPI was significantly more frequent in patients with liver cirrhosis than those without, but Hcy level and proportions of HHcy and positive aCL were not significantly different between them. PVST could be evaluated in 136 cirrhotic patients. Hcy level [10.57 µmol/L (2.71-56.82) versus 9.97 µmol/L (2.05-53.44); P = 0.796] and proportions of HHcy [4/44 (9.1%) versus 13/81 (16.0%); P = 0.413] and positive aCL [1/23 (4.3%) versus 10/52 (19.2%); P = 0.185] and aß2GPI [9/23 (39.1%) versus 21/52 (40.4%); P = 0.919] were not significantly different between cirrhotic patients with and without PVST. There was still no significant association of Hcy level, HHcy, aCL, or aß2GPI with PVST based on Child-Pugh classification, MPV thrombosis >50%, and clinically significant PVST. Hcy, aCL, and aß2GPI may not be associated with PVST in liver cirrhosis, suggesting that routine screening for Hcy, aCL, and aß2GPI should be unnecessary in such patients.

Autoimmune haemolytic anaemia and thrombocytopaenia in a single-centre cohort of patients with systemic lupus erythematosus from Turkey: clinical associations and effect on disease damage and survival.

INTRODUCTION: Thrombocytopaenia and autoimmune haemolytic anaemia (AIHA) have considerable impact on prognosis in systemic lupus erythematosus (SLE). We investigated the frequencies of these haemocytopaenias, along with their associations and effect on outcome in a single-centre cohort of patients with SLE. METHODS: Demographic characteristics, clinical features, autoantibody profiles, damage and mortality data were compared between patients with and without each haematological abnormality. Variables displaying significant differences between the groups were entered into logistic regression. RESULTS: Ninety-three patients had AIHA and 215 had thrombocytopaenia. Both were associated with neuropsychiatric (NP) involvement, with each other, leucopaenia, antiphospholipid syndrome (APS) and antiphospholipid antibodies. More patients in both groups had organ damage, and their damage scores were higher. Association to NP damage was discernible. In addition, cardiovascular and renal damage and diabetes were more pronounced in patients with thrombocytopaenia. At logistic regression analysis, younger age, anticardiolipin antibody IgM positivity, leucopaenia and thrombocytopaenia were associated with AIHA whilst lupus anticoagulant activity, AIHA, leucopaenia, APS and NP involvement were associated with thrombocytopaenia. Among damage items, peripheral vascular damage, diabetes, NP damage, renal and ocular damage displayed significant associations with thrombocytopaenia, whereas none of the items did with AIHA. Patients with AIHA had significantly reduced survival rates at 10 and 20 years. CONCLUSIONS: We observed that AIHA and thrombocytopaenia were associated with severe lupus, affecting major organs and causing end organ damage. Thus, they may be considered as prognostic markers. Furthermore, AIHA and especially thrombocytopaenia may also be a marker for a subgroup of lupus patients who have or may develop APS.

Renal protective effect of antiplatelet therapy in antiphospholipid antibody-positive lupus nephritis patients without antiphospholipid syndrome.

OBJECTIVE: We sought to evaluate the effect of antiplatelet therapy in addition to conventional immunosuppressive therapy for lupus nephritis (LN) patients positive for antiphospholipid antibodies (aPL) without definite antiphospholipid syndrome (APS). METHODS: Patients with biopsy-proven LN class III or IV were retrospectively evaluated. We selected patients positive for anticardiolipin antibody (aCL) or lupus anticoagulant (LA) who did not meet the criteria for a diagnosis of APS. The patients were divided into two subgroups according to whether antiplatelet therapy was received. The cumulative complete renal response (CR) rate, relapse-free rate, and change in estimated glomerular filtration rate (eGFR) over 3 years after induction therapy were calculated. RESULTS: We identified 17 patients who received antiplatelet therapy and 21 who did not. Baseline clinicopathological characteristics and immunosuppressive therapy did not show a significant difference between the two groups except for a higher incidence of LN class IV in the treatment group (p = 0.03). There was no difference in cumulative CR rate, relapse-free rate, or eGFR change between these subgroups. However, when data on LA-positive patients were assessed, an improvement in eGFR was found (p = 0.04) in patients receiving antiplatelet treatment. CONCLUSION: Addition of anti-platelet therapy was associated with an improvement of eGFR in LA-positive patients with LN class III or IV.

Plasma Antiphospholipid Antibodies Effects on Activated Partial Thromboplastin Time Assays.

BACKGROUND: Activated partial thromboplastin time (aPTT) assays can be affected by plasma antiphospholipid antibodies (aPLs), but the degree of the interference is not easy to predict. This study aimed to investigate the effects on aPTT assay results of different types and combinations of aPLs, including anti-ß2-glycoprotein I antibodies, anticardiolipin antibodies and lupus anticoagulant. MATERIALS AND METHODS: We retrospectively collected clinical information and laboratory tests from aPL-positive patients. The potential influence of aPLs on aPTT assays was assessed. RESULTS: The survey included 589 aPL-positive patients. No significant differences existed in basic characteristics such as sex, age, prothrombin time, fibrinogen and alanine aminotransferase among different cases with 1, 2 or 3 types of positive-aPL markers (P > 0.05). In 113 patients with abnormal aPTT values, multivariable linear regression analysis showed a significant correlation between an abnormal degree of aPTT values and dilute Russell viper venom time (dRVVT) or silica clotting time (SCT) with a correlation coefficient of 0.437 or 0.497 (P < 0.01), whereas age, anticardiolipin antibodies-immunoglobulin G, anticardiolipin antibodies-immunoglobulin M and anti-ß2-glycoprotein I antibodies were of no significance (P > 0.05). Among blood samples with 3 types of aPLs positivity, the rate of abnormal aPTT detection values was 55.3%, which was significantly higher than that observed in patients with negative, single-positive or double-positive aPL markers (P < 0.05). Patients with a moderate to strong dRVVT or SCT had a higher proportion of abnormal aPTT assays than did patients with a low dRVVT or SCT (P < 0.05). CONCLUSIONS: When abnormal aPTT values are obtained, the influence of aPLs should be considered, especially in the presence of a moderate to strong dRVVT or SCT.

Comparison of different enzyme-linked immunosorbent assay methods for avidity determination of antiphospholipid antibodies.

BACKGROUND: Avidity of antiphospholipid antibodies may be clinically useful as a valuable additional characteristic. The aim of this study was to compare several ELISA modifications with different chaotropic agents and calculation of avidity indices for the determination of anticardiolipin antibody (aCL) avidity. METHODS: We examined 28 serum samples with positive IgG aCL by adapted ELISA using various concentrations of urea and sodium chloride as chaotropic agents and different dilution of sera. We tested these conditions of ELISA-a single diluted serum sample with fixed concentration of a chaotrope and a serially diluted serum in the constant concentration of a chaotropic agent. RESULTS: We demonstrated that ELISA method for avidity determination based on a single dilution of serum in the presence of fixed concentration of chaotrope is convenient for determination of IgG aCL antibody avidity. Concentrations 6 and 8 mol/L of urea or 1 and 2 mol/L of NaCl were suitable for sufficient dissociation of immune complexes during ELISA procedure. CONCLUSION: This way was in good agreement with more demanding procedures. Both urea and sodium chloride may be used as chaotropic agents. Reference values of avidity indices essential for interpretation of patients' results must be established individually for distinct assay conditions.

Significance of fully automated tests for the diagnosis of antiphospholipid syndrome.

Antiphospholipid antibodies (aPLs) can vary both immunologically and functionally, thus it is important to effectively and correctly identify their presence when diagnosing antiphospholipid syndrome. Furthermore, since many immunological/functional tests are necessary to measure aPLs, complete examinations are often not performed in many cases due to significant burden on the testing departments. To address this issue, we measured aPLs defined according to the classification criteria (anticardiolipin antibody: aCL) IgG/IgM and anti-ß2 glycoprotein I antibody (aß2GPI) (IgG/IgM) as well as non-criteria antibodies (aCL IgA, aß2GPI IgA and aß2GPI domain I), in a cohort of 211 patients (61 APS, 140 disease controls and 10 healthy individuals). APLs were measured using a fully automated chemiluminescent immunoassay instrument (BIO-FLASH®/ACL AcuStar®) and with conventional ELISA tests. We demonstrated that both sensitivity and accuracy of diagnosis of aCL IgG and aß2GPI IgG were high, in agreement with the past reports. When multiple aPLs were examined, the accuracy of diagnosis increased. The proportion of APS patients that were positive for 2 or more types of aPLs (47/61, 77%) was higher than that of patients with systemic lupus erythematosus (SLE)(3/37, 9%), those with non-SLE connective tissues diseases (1/53,2%), those with other diseases or healthy volunteers. Based on these findings, it was concluded that the fully automated chemiluminescent immunoassay instrument, which allows the simultaneous evaluation of many types of aPLs, offers clear advantages for a more complete, more rapid and less labor-intensive alternative to running multiple ELISA and could help in better diagnosis for suspected APS patients.

Role of apolipoprotein B100 and oxidized low-density lipoprotein in the monocyte tissue factor induction mediated by anti-ß2 glycoprotein I antibodies.

OBJECTIVE: The objective of this paper is to elucidate the not yet known plasma molecule candidates involved in the induction of tissue factor (TF) expression mediated by ß2GPI-dependent anticardiolipin antibody (aCL/ß2GPI) on monocytes. METHODS: Human serum incubated with FLAG-ß2GPI was applied for affinity chromatography with anti- FLAG antibody. Immunopurified proteins were analyzed by a liquid chromatography coupled with mass spectrometry (LC-MS). TF mRNA induced by the identified molecules on monocytes was also analyzed. RESULTS: Apolipoprotein B100 (APOB) was the only identified serum molecule in the MS search. Oxidized LDL, containing APOB as well as ox-Lig1 (a known ligand of ß2GPI), was revealed as a ß2GPI-binding molecule in the immunoprecipitation assay. TF mRNA was markedly induced by oxidized LDL/ß2GPI complexes with either WBCAL-1 (monoclonal aCL/ß2GPI) or purified IgG from APS patients. The activities of lipoprotein-associated phospholipase A2, one of the component molecules of oxidized LDL, were significantly higher in serum from APS patients than in those from controls. CONCLUSION: APOB (or oxidized LDL) was detected as a major ß2GPI binding serum molecule by LC-MS search. Oxidized LDL/aCL/ß2GPI complexes significantly induced TF expressions on monocytes. These data suggest that complexes of oxidized LDL and aCL/ß2GPI may have a crucial role in the pathophysiology of APS.

Elevated levels of antibodies against phosphatidylserine/prothrombin complex and/or cardiolipin associated with infection and recurrent purpura in a child: a forme fruste of antiphospholipid syndrome?

Antiphospholipid syndrome is an autoimmune disorder characterized by the occurrence of venous and arterial thrombosis, as well as morbidity in pregnancy, in the presence of anti-phospholipid antibodies. The diagnosis of antiphospholipid syndrome is usually established based on clinical and laboratory findings by strictly following the 2006 Sapporo classification. However, the diagnosis remains challenging owing to the ongoing debates on the serological criteria. We report a case we describe as forme fruste antiphospholipid syndrome in which these criteria were not fulfilled. Purpura appeared repeatedly in a female infant starting from the age of 6 months and following episodes of upper respiratory infections and vaccinations. The levels of anti-cardiolipin IgG antibodies and anti-phosphatidylserine/prothrombin complex antibodies were elevated in accordance with these events. Histopathological evaluation revealed multiple small vessel thrombi in the dermis and adipose tissue. After 2 weeks of treatment with aspirin and heparin, the cutaneous symptoms subsided. Infection has long been associated with antiphospholipid syndrome, and anti-phosphatidylserine/prothrombin antibodies are considered a new marker for the diagnosis of antiphospholipid syndrome. Forme fruste antiphospholipid syndrome should be considered even if the antiphospholipid syndrome diagnostic criteria are not completely fulfilled, especially in the presence of elevated levels of anti-phosphatidylserine/prothrombin antibodies and known preceding infections.

Cutaneous manifestations in antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is a hypercoagulable state that leads to thrombosis and recurrent pregnancy loss related to the presence of antiphospholipid antibodies (LAC, anticardiolipin, antiA2-glycoprotein). Among cutaneous manifestations, livedo reticularis is the most frequent form of APS. In the literature, there are rare cases associated with diffuse skin necrosis (widespread skin necrosis) and intravascular thrombosis in the small vessels of the dermis. We describe the case of a 44-year-old man with positive anticardiolipin antibodies and protein S deficiency that developed scattered, bullous skin lesions, haemorrhagic in appearance with signs of necrosis as first clinical manifestation of antiphospholipid syndrome.

Antiphospholipid antibody and risk of retinal vein occlusion: a systematic review and meta-analysis.

BACKGROUND: Retinal vein occlusion (RVO) is a common retinal vascular disease and it is one of the most frequently reported causes of visual damage and blindness in the elderly. The current study investigated the potential association between antiphospholipid antibodies (APLA) and RVO risk by conducting a meta-analysis of case-control studies. METHODS: A systematic literature search of Pubmed and Embase databases was conducted in August 1st, 2014. Odds ratios (ORs) were used to evaluate the associations between APLA and the incidence of RVO. A random-effects model was obtained for the quantitative synthesis. RESULTS: A total of 11 studies were included in this meta-analysis. A meta-analysis of all studies assessing the risk of RVO revealed that APLA was associated with a statistically increased risk of RVO incidence (OR = 5.18, 95% CI = [3.37, 7.95]). The association between anticardiolipin antibodies (ACA) and the risk of RVO was significant (n =8, OR = 4.59, 95% CI = [2.75, 7.66]). However, the association between lupus anticoagulants (LA) and risk of RVO was non-significant (n = 5, OR = 3.90, 95% CI = [0.99, 15.37]). No significant publication bias was found in the 11 selected studies. CONCLUSION: APLA was significantly associated with the risk of RVO. Advanced analyses showed that ACA rather than LA affected the risk of RVO. Additional well-designed and well-conducted epidemiological studies are required to further our understanding of the relationship between APLA and RVO risk.

Klinefelter's syndrome and venous thrombosis.

Klinefelter's syndrome is the most common cause of primary testicular failure. Previous reports have associated Klinefelter's syndrome with increased risk of thrombosis. The exact cause for this association is unknown, but hypoandrogenism affecting fibrinolysis has been implicated. The authors described a unique patient with Klinefelter's syndrome who presented with deep vein thrombosis of the leg and underlying mutations of MTHFR gene, increased factor VIII coagulant activity and an elevated anticardiolipin antibody. To the authors' knowledge, this combination of hypercoagulability risk factors in such a patient has not been previously reported. The authors also reviewed previously published reports of similar patients and discuss potential genetic mutations that may in part predispose this group of patients to venous thrombosis.

Effects of anti-cardiolipin antibodies and IVIg on annexin A5 binding to endothelial cells: implications for cardiovascular disease.

OBJECTIVES: Anti-phospholipid antibodies (aPL), including anti-cardiolipin antibodies (aCL), are risk factors for cardiovascular disease (CVD) in the general population and in patients with the anti-phospholipid syndrome (APS; Hughes syndrome). APS may be primary but is also common in patients with systemic lupus erythematosus (SLE). The anti-coagulant protein annexin A5 (ANXA5) is implicated in CVD by interfering with phospholipids and aPL. METHODS: ANXA5 binding to human umbilical venous endothelial cells (HUVECs) was determined by flow cytometry. RESULTS: When cells were cultured in serum from APS patients with a high aPL titre (aPL-S), binding of ANXA5 to HUVECs was reduced. Monoclonal immunoglobulin (Ig)G aPL against cardiolipin (mAb-CL) dose-dependently reduced ANXA5 binding to endothelium. Preincubation of intravenous (IV)Ig at therapeutically relevant doses with aPL-S and mAb-aCL restored ANXA5 binding to comparable levels when normal healthy serum (NHS) was used. By contrast, IVIg per se had the capacity to reduce ANXA5 binding to endothelium when added to NHS (but not to aPL-S). CONCLUSIONS: Decreased ANXA5 binding to endothelium, mediated by aPL, is a novel mechanism of atherothrombosis that can be countered by IVIg in vitro. IVIg per se could, to a lesser degree, cause decreased ANXA5 binding in NHS, which raises the possibility that some antibodies in IVIg can be involved in a side-effect reported in IVIg treatment, namely atherothrombosis and CVD. Increasing ANXA5 binding, either by addition of ANXA5 or by use of neutralizing antibodies in IVIg, represents a possible therapeutic strategy that deserves further study.

[The role of angelica injection on P-selectin and anti-cardiolipin antibodies in acute pulmonary embolism rats].

OBJECTIVE: To study the effect of Chinese medicine, Angelica, injection on the expression of P-, E-selectin and anti-cardiolipin antibody in acute pulmonary embolism rats. METHODS: SD rats were randomly divided into 3 groups: normal control group(Group N), thromboembolism group (Group T), and treatment group of thromboembolism with angelica injection (Group TA). There were three time points in every group: 1 h, 4 h and 8 h. Plasma was detected by P-, with 4% paraformaldehyde, and paraffin embedded sections were detected by immunohistochemistry for P-, E-selectin and anti-cardiolipin antibodies. RESULTS: With HE stain, the inflammatory cells in the lung of rats were relatively rare in every time point in normal control group. In group T and group TA, the inflammatory cells were increasing in every time point in comparison to group N (P < 0.05) and the inflammatory cells were increasing with time in group T. The data revealed that the plasmic level of P-, E-selectin was significantly higher than that in group T1, group T4, group T8 in comparison to the corresponding sub groups of group N (P < 0.05), while it was significantly lower than that in group TA1, group TA4, group TA8 in comparison to the corresponding sub groups of group T (P < 0.05); For the OD value of plasmic anti-cardiolipin antibodies (ACA), no significant difference was observed during was lower expressed by immunohistochemistry. CONCLUSION: Acute pulmonary embolism can lead to infiltration of inflammatory cell in rat lungs. The lung inflammation of acute pulmonary embolism rats can be enhanced probably by the increased release of P-, E-selectin and anti-cardiolipin antibodies, and the enhanced inflammation promotes the release of a series of inflammatory mediators, which exacerbate the injury of lung. Angelica injection relieves the lung inflammation of acute pulmonary embolism rats possibly by inhibiting the expression of P-, E-selectin and anti-cardiolipin antibody, thus playing a role in reducing thrombogenesis.

Plasmin immunization preferentially induces potentially prothrombotic IgG anticardiolipin antibodies in MRL/MpJ mice.

OBJECTIVE: To test the hypothesis, utilizing 2 experimental mouse models, that plasmin is an important autoantigen that drives the production of certain IgG anticardiolipin (aCL) antibodies in patients with the antiphospholipid syndrome. METHODS: BALB/cJ and MRL/MpJ mice were immunized with Freund's complete adjuvant in the presence or absence of human plasmin. The mouse sera were analyzed for production of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)-glycoprotein I (anti-beta(2)GPI) antibodies. IgG monoclonal antibodies (mAb) were generated from the plasmin-immunized MRL/MpJ mice with high titers of aCL, and these 10 mAb were studied for their binding properties and functional activity in vitro. RESULTS: Plasmin-immunized BALB/cJ mice produced high titers of IgG antiplasmin only, while plasmin-immunized MRL/MpJ mice produced high titers of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)GPI. Both strains of mice immunized with the adjuvant alone did not develop IgG antiplasmin or IgG aCL. All 10 of the IgG mAb bound to human plasmin and cardiolipin, while 4 of 10 bound to beta(2)GPI, 3 of 10 bound to thrombin, and 4 of 10 bound to the activated coagulation factor X (FXa). Functionally, 4 of the 10 IgG mAb inhibited plasmin activity, 1 of 10 hindered inactivation of thrombin by antithrombin III, and 2 of 10 inhibited inactivation of FXa by antithrombin III. CONCLUSION: Plasmin immunization leads to production of IgG antiplasmin, aCL, and anti-beta(2)GPI in MRL/MpJ mice, but leads to production of only IgG antiplasmin in BALB/cJ mice. IgG mAb generated from plasmin-immunized MRL/MpJ mice bind to various antigens and exhibit procoagulant activity in vitro. These results suggest that plasmin may drive potentially prothrombotic aCL in genetically susceptible individuals.

[Concetration of anticardiolipin antybodies in peritonel fluid and in fluid from lymphocytes culture in women with endometriosis]. / Stezenie przeciwcial antykardiolipinowych w plynie otrzewnowym i w plynie z hodowli limfocytów kobiet z endometrioza.

AIM: The aim of our work was to study both the concentration of anticardiolipin antibodies (aCL) in peritoneal fluid in women with endometriosis and to examine peritoneal lymphocyte ability to produce anticardiolipin antibodies. MATERIAL AND METHODS: Study group included 30 women with endometriosis. The clinical stages of the disease were assessed by the revised American Fertility Society (rAFS) classification. Reference group included fifteen healthy women, with excluded endometriosis and other pathological disorders within the pelvis. The concentration of aCL in the peritoneal fluid and in fluid from lymphocyte culture was measured by enzyme-linked immunosorbent ELISA assay. RESULTS: Statistical analysis showed significantly increased mean concentration of aCL in peritoneal fluid in women with endometriosis compared to women from the reference group (p<0.0001). The concentration of aCL in fluid from lymphocyte culture was also significantly higher in samples from women with endometriosis than from the reference group (p<0.0001). The highest mean levels of aCL in peritoneal fluid and in fluid from lymphocyte culture were observed in samples from women with stage I of the disease. CONCLUSIONS: An increased level of anticardiolipin antibodies in peritoneal fluid in women with endometriosis and increased antibodies production by lymphocytes may suggest an impairment of humoral immunity and its intensification in the early stages of the disease.

Associação entre anticorpos antifosfolípides e fator reumatóide empacientes com nefrite lúpica: um estudo de 187 casos / Associatiom between antiphospholipid antibodies and rheumatoid factor in patients with Lupus Nephrits: a study of 187 cases

Introdução: Nefrite é uma manifestação freqüente no lúpus eritematoso sistêmico (LES), tendo uma prevalência de 40 a 75%. Embora esteja associada com a ocorrência de anticorpo anti-DNA, outros autoanticorpos podem estar ligados ao seu aparecimento taiscomo o fator reumatóide (FR) e os anticorpos antifospholípides (aPl).Objetivos: verificar a prevalência de nefrite lúpica local e sua associação com o a presença do FR e aPls. Métodos: Revisaram-se 187 prontuários depacientes com LES para presença de nefrite, FR e aPl . Resultados: Encontrou-se uma prevalência de 35,3% de glomerulonefrite. Houve correlação negativa entre nefrite e FR (p=0.001). Não se encontrou associação entre aparecimento de aPl e nefrite, já queo número de pacientes com glomerulonefrite que apresentaram esses testes positivos foram de 8 (32%)em 59; 5 (27,7%) em 58 e 6 (46,1%) em 29, respectivamente. Conclusão: Existe uma prevalência de 35% denefrite na população local de LES a qual tem uma associação negativa com aparecimento do FR. Presença de aPls não influíram no aparecimento da nefrite lúpica.

Summary: Nephritis is a frequent manifestation of systemic lupus erythematosus (SLE), with an averageof 40 to 75%. It’s associated with the presence of anti-DNA antibodies;other antibodies may also be involved,such as rheumatoid factor (RF), and antiphospholipid antibodies (aPl).Objectives: to verify the prevalence of lupus nephritis and its association with RF and aPl antibodies. Methods: The charts of 187 patients with SLE werereviewed for the presence of nephritis, RF and aPl. Results: A prevalence of 35.3% of nephritis was found. There was a negative correlation betweennephritis and presence of rheumatoid factor (p=0,001). No association between the presence of aPl and nephritis was found, since the number of patients with glomerulonephritis that were positive for these tests wasof 8 (32%) in 59, 5 (27,77%) in 58 and 6 (46,1%) in 29, respectively.Conclusion: There is a prevalence ofglomerulonephritis of 35% in the local SLE population, which has a negative association with rheumatoid factorpresence. Antiphospholipid antibodies aren’t associated to the occurrence of lupus nephritis.