Anti-endothelial Cell Antibodies Research Articles

Autoantibody profile in children with Kawasaki disease on long-term follow-up: A prospective study from North India.

To study the profile of autoantibodies on long-term follow-up of children with Kawasaki disease (KD). In this single-center observational cohort study, 50 children who had been diagnosed and treated for KD with a minimum follow-up period of 3years were enrolled. The organ-specific autoantibodies that were assessed in the study included anti-thyroid microsomal antibody (TMA), anti-parietal cell antibody (PCA) and anti-liver kidney microsomal (LKM) antibody. The organ-nonspecific autoantibodies that were studied included anti-endothelial cell antibody (AECA), anti-nuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), anti-mitochondrial antibody (AMA) and anti-smooth muscle antibody (SMA). The sample for assessment of serology was taken at a mean follow-up period of 6.41years (±1.95 SD) after diagnosis. Autoantibodies were detected in 11/50 (22%) patients. ANA was detected in three patients, TMA was positive in seven and ANCA was positive in one. These autoantibodies likely develop in children with KD during the acute stage and may persist for many years. There is no concrete evidence to suggest that these children are at increased risk of developing an autoimmune disease in the future. However, there is some justification for prolonged surveillance for development of autoimmune manifestations.

Anti-endothelial cell antibody rich sera from rheumatic heart disease patients induces proinflammatory phenotype and methylation alteration in endothelial cells

Rheumatic heart disease (RHD) is a major cause of cardiovascular morbidity and mortality in developing nations like India. RHD commonly affects the mitral valve which is lined by a single layer of endothelial cells (ECs). The role of ECs in mitral valve damage during RHD is not well elucidated. In here, anti-endothelial cell antibody from RHD patients has been used to stimulate the ECs (HUVECs and HMVECs). ECs proinflammatory phenotype with increased expression of TNFα, IL-6, IL-8, IFNγ, IL-1β, ICAM1, VCAM1, E-selectin, laminin B, and vimentin was documented in both ECs. The promoter hypomethylation of various key inflammatory cytokines (TNFα, IL-6, and IL-8), integrin (ICAM1) associated with leukocyte transendothelial migration, and extracellular matrix genes (vimentin, and laminin) were also observed. Further, the in-vitro data was in accordance with ex-vivo observations which correlated significantly with the etiological factors such as smoking, socioeconomic status, and housing. Thus, the study sheds light on the role of ECs in RHD which is a step forward in the elucidation of disease pathogenesis.

Pre-transplant Screening for Non-HLA Antibodies: Who should be Tested?

Retrospective studies of angiotensin II type 1 receptor antibodies (AT1R-Ab) and anti-endothelial cell antibodies (AECA) have linked these antibodies to allograft injury. Because rising healthcare costs dictate judicious use of laboratory testing, we sought to define characteristics of kidney transplant recipients who may benefit from screening for non-HLA antibodies. Kidney recipients transplanted between 2011 and 2016 at Johns Hopkins, were evaluated for AT1R-Ab and AECA. Pre-transplant antibody levels were compared to clinical and biopsy indications of graft dysfunction. Biopsies were graded using the Banff' 2009–2013 criteria. AT1R-Ab and AECA were detected using ELISA and endothelial cell crossmatches, respectively. AT1R-Ab levels were higher in patients who were positive for AECAs. Re-transplanted patients (p < 0.0001), males (p = 0.008) and those with FSGS (p = 0.04) and younger (p = 0.04) at time of transplantation were more likely to be positive for AT1R-Ab prior to transplantation. Recipients who were positive for AT1R-Ab prior to transplantation had increases in serum creatinine within 3 months post-transplantation (p < 0.0001) and developed abnormal biopsies earlier than did AT1R-Ab negative patients (126 days versus 368 days respectively; p = 0.02). Defining a clinical protocol to identify and preemptively treat patients at risk for acute rejection with detectable non-HLA antibodies is an important objective for the transplant community.

Anti-endothelial cell antibodies do not correlate with disease activity in systemic sclerosis.

IntroductionAnti-endothelial cell antibodies (AECA) recognize endothelial cell proteins and are thought to play an important role in vascular damage observed in systemic scleroderma (SSc) and many other autoimmune diseases. In SSc, AECA were found to be more common in patients with pulmonary hypertension, digital ulcers and nailfold capillaroscopic changes. Until now, there have been no studies examining the association between AECA positivity with the activity and duration of the disease.AimTo evaluate associations between the presence of AECA in sera of patients with SSc and internal organs involvement as well as disease activity.Material and methodsSera of 58 patients with SSc (50 with localized subtype and 8 with diffuse subtype) were examined for AECA presence using an indirect immunofluorescence technique. Several clinical and laboratory features were also evaluated as well as disease activity and disease duration.ResultsA significant association between positive AECA and a subtype of SSc (p = 0.021) was found, as well as between presence of digital ulcers and digital scars (p = 0.001), calcinosis (p = 0.02), acroosteolysis (p = 0.028) and a nearly significant association between AECA and lung fibrosis (p = 0.47). No association between disease duration, disease activity and AECA (p = 1.000 and 0.191, respectively) was present.ConclusionsAnti-endothelial cell antibodies are not associated with the activity of SSc. Digital ulcers, calcinosis and acroosteolysis are more common among AECA-positive patients suggesting that the presence of AECA might be an indicator of vascular complications development in SSc. Positive AECA among patients with lung fibrosis indicate their possible role in the development of lung disease. Further prospective studies including a greater number of patients are required.

The clinical significance of detection of the anti-endothelial cell antibodies in sera from children with Kawasaki disease

The clinical significance of detection of the anti-endothelial cell antibodies in sera from children with Kawasaki disease

Antiendothelial cell antibodies as the tip of the iceberg: What is hidden underneath?

A system analysis of the published data on antiendothelial cell antibodies (AECAs) was performed. The AECAs target antigens on endothelial cells are characterized, the methodology of revealing AECAs is described, and the role of antibodies in the pathogenesis of processes caused by the activation/dysfunction of endothelium is considered. The review summarizes the present-day results of Russian and international studies published in the last 25 years in the Pubmed, High Wire, and e-Library databases. The characteristics of natural and disease-associated AECAs (related to pathology) and mechanisms of their influence on cells in different pathologies are presented.

OR48 Antibodies against vascular endothelial keratin 1 antigen associate with deterioration of renal allograft function

Aim Non-HLA antigens have been found to involve in organ transplant rejection. Studies have shown that most of non-HLA antigens are targets of anti-endothelial cell antibodies (AECAs) and paly role on the antibody-mediated rejection (AMR), but these antigens on the surface of endothelial cells (EC) are not yet fully identified. Methods In this study, we isolated the anti-EC specific antibodies (IgG) for the serum AECAs of renal allograft recipients with antibody adsorption and elution by human endothelial cells. The response antigen(s) were captured via immunoprecipitation using AECA obtained. Results Mass spectrometry analysis showed that the endothelia antigen Keratin-1 (KRT1) was frequently found as the target transplant antigen. Three most common KRT1 alleles were cloned, expressed and purified, using KRT1 antigens as antigens we developed an ELISA to detect anti-KRT1 antibodies in the patients with renal transplantation. The results showed that the positive rate of serum KRT1 antibodies was 20.8% (53/255) in the renal transplant recipients. Further analysis of the specificity of the anti-KRT1 antibodies and recipient’s KRT1 genotype showed that 89.3% of the patients produced anti-KRT1 antibodies that reacted with their own KRT1 antigen, suggesting that the anti-KRT1 antibodies likely belong to autoantibodies. The recipients of renal transplantation were divided into two groups according to the serum creatinine (Cr) levels. Anti-KRT1 antibodies (IgG) were detected in 29.9% (23/77) recipients with Cr > 120 μmol/L, while, it was 16.9%(30/178) in kidney transplant recipients with Cr⩽120 μmol/L. The difference is statistically significant (x 2 = 5.531, P Conclusions Anti-KRT1 antibodies are associated with the deterioration of renal graft function after transplantation. Detection of anti-KRT1 IgG might be beneficial for the recipients after renal transplantation.

P1789Elevated antiendothelial cell antibodies are associated with higher likelihood of normal coronary angiograms

P1789Elevated antiendothelial cell antibodies are associated with higher likelihood of normal coronary angiograms

Pattern of antiendothelial cell antibodies in patients with chronic obstructive pulmonary disease

BackgroundAutoimmune mechanisms have been recently recognized as being partly involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Circulating autoantibodies have been detected in patients with COPD.ObjectivesThe aim of this study was to estimate the level of antiendothelial cell antibodies (AECA) in COPD patients in the various GOLD stages.Patients and methodsA comparative study assessed the level of AECA in three groups. COPD patients without cor pulmonale (18), with cor pulmonale (12), and the control group (10), from Beni-Suef University Hospital. Each group underwent background questionnaires and BMI measures. Enzyme-linked immunosorbent assay was used to measure the level of AECA in serum (ng/ml). Right ventricular systolic pressure (mm Hg) was measured in COPD patients with cor pulmonale.ResultsThe studied groups consisted of male patients (age: 50–80 years). BMI was significantly lower (20.36) in the COPD group with cor pulmonale. Spirometry forced expiratory volume and forced expiratory volume/forced vital capacity ratios showed significantly lower levels among the COPD patients without cor pulmonale. AECA showed a lower level in the control group (26.25) compared with the COPD without cor pulmonale (57.87) and much lowered when compared to cor pulmonale group (71.47). The level of AECD was higher in the patients in third (74.78) and fourth stages (79.10) compared with those in the second stage (58.75).ConclusionThere is a much higher level of AECA in COPD patients with cor pulmonale and in advanced stages in comparison with patients without cor pulmonale and at early stages, and a significant positive correlation was found between AECA levels and right ventricular systolic pressure.

The role of endothelial cells in the vasculopathy of systemic sclerosis: A systematic review.

Systemic sclerosis (SSc) is an autoimmune connective tissue disorder characterized by fibroproliferative vasculopathy, immunological abnormalities and progressive fibrosis of multiple organs including the skin. In this study, all English speaking articles concerning the role of endothelial cells (ECs) in SSc vasculopathy and representing biomarkers are systematically reviewed and categorized according to endothelial cell (EC) (dys)function in SSc. A sensitive search on behalf of the EULAR study group on microcirculation in Rheumatic Diseases was developed in Pubmed, The Cochrane Library and Web of Science to identify articles on SSc vasculopathy and the role of ECs using the following Mesh terms: (systemic sclerosis OR scleroderma) AND pathogenesis AND (endothelial cells OR marker). All selected papers were read and discussed by two independent reviewers. The selection process was based on title, abstract and full text level. Additionally, both reviewers further searched the reference lists of the articles selected for reading on full text level for supplementary papers. These additional articles went through the same selection process. In total 193 resulting articles were selected and the identified biomarkers were categorized according to description of EC (dys)function in SSc. The most representing and reliable biomarkers described by the selected articles were adhesion molecules for EC activation, anti-endothelial cell antibodies for EC apoptosis, vascular endothelial growth factor (VEGF), its receptor VEGFR-2 and endostatin for disturbed angiogenesis, endothelial progenitors cells for defective vasculogenesis, endothelin-1 for disturbed vascular tone control, Von Willebrand factor for coagulopathy and interleukin (IL)-33 for EC-immune system communication. Emerging, relatively new discovered biomarkers described in the selected articles, are VEGF165b, IL-17A and the adipocytokines. Finally, myofibroblasts involved in tissue fibrosis in SSc can derive from ECs or epithelial cells through a process known as endothelial-to-mesenchymal transition. This systematic review emphasizes the growing evidence that SSc is primarily a vascular disease where EC dysfunction is present and prominent in different aspects of cell survival (activation and apoptosis), angiogenesis and vasculogenesis and where disturbed interactions between ECs and various other cells contribute to SSc vasculopathy.

Silicosis and autoimmunity.

Of the various environmental, occupational, and medical substances that cause dysregulation of autoimmunity, the effects and causative mechanisms of silica particles and asbestos fibers are discussed in this review. With respect to silica, many epidemiological studies have shown a significant association between silica exposure and the occurrence of autoimmune diseases. Although the importance of the NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome as the initial immune reaction against silica particles has been identified, the mechanisms involved that lead to various autoimmune diseases in patients exposed to silica remain largely unknown. Silica can activate various immune cells and investigation of the associated imbalance of regulatory T cells, responder T cells as well as Th17 cells might be key in furthering our understanding of silica-induced autoimmune alterations. On the other hand, asbestos exposure shows less association with autoimmune diseases. However, interesting findings pertaining to the detection of antiendothelial and mesothelial cell antibodies in asbestos-exposed patients have been reported. Taken together, further investigations may contribute in delineating the mechanisms involved in environmental factor-induced modification of autoimmunity.

Assessing the potential of angiotensin II type 1 receptor and donor specific anti-endothelial cell antibodies to predict long-term kidney graft outcome

Endothelial cell antigens have been reported as potential targets for antibodies in the context of organ transplantation, leading to increased risk for graft failure. Serum samples from 142 consecutive living donor kidney recipients were tested for the presence of antibodies to angiotensin II – type 1 receptor (AT1R), donor endothelial cells, and donor HLA. Graft survival was monitored for five years post-transplant, and secondary outcomes, including biopsy-proven rejection, proteinuria, biopsy-proven vasculopathy, and renal function based on serum creatinine were also assessed for the first two to three years. AT1R antibody levels were positive (>17U/mL) in 11.3%, 18.8% and 8.1% of patients pre-transplant, post-transplant and at time of indication biopsy, respectively. XM-ONE assay was positive in 17.6% of patients pre-transplant (7 IgG+; 15 IgM+; 3 IgG+/IgM+). Overall, 4 patients experienced antibody-mediated rejection (AMR), 31 borderline cellular rejection (BCR), 19 cellular rejection (CR) and 3 mixed AMR and CR within the first 24months. While pre-existing and de novo donor-specific HLA antibodies were associated with graft failure and many secondary outcomes, no statistical association was found for either anti-endothelial or anti-AT1R antibodies, indicating that these tests may not be the best predictors of graft outcome in living donor renal transplantation.

Analysis of Sera of Recipients with Allograft Rejection Indicates That Keratin 1 Is the Target of Anti-Endothelial Antibodies.

Anti-endothelial cell antibodies (AECAs) are usually directed against the surface antigens on the vascular endothelial cells. Clinical studies suggest a pathogenic role for nonhuman leukocyte antigen in antibody-mediated rejection; however, the antigens on the donor vascular endothelium that serve as the first-line targets for an immune response during allograft rejection have not been fully identified. Here, we used immunoprecipitation and mass spectrometry to identify antigens from the sera of kidney transplant recipients who were experiencing antibody-mediated rejection. Keratin 1 (KRT1) was identified as a novel antigenic target expressed on endothelial cells. To validate our finding, we produced recombinant proteins representing the three most common alleles of KRT1. The serum used for immunoprecipitation showed a strong reaction to KRT1 recombinants in western blot and ELISA. In the kidney transplant cohort, more AECA-positive recipients than AECA-negative recipients had KRT1 antibodies (32.2% versus 11.9%, p = 0.002). Sera from 255 renal recipients were tested by ELISA. Of the 77 recipients with deteriorating graft function (serum creatinine > 120 μmol/L), 23 had anti-KRT1 antibodies. KRT1-IgG positivity was, therefore, associated with a higher risk of kidney transplant rejection (29.9% (23/77) versus 16.9% (30/178), p = 0.0187). A better understanding of this antigenic target will improve long-term allograft survival.

THROMBOTIC AND THROMBOEMBOLIC COMPLICATIONS IN SYSTEMIC VASCULITIS

Nowadays, there is no doubt about the relationship between immune inflammation and the development of thrombosis due to the similarity of many pathogenetic machanisms underlying both pathological processes. Systemic vasculitis, along with other immuno- mediated inflammatory diseases, represent one of the most clear examples of such interaction. Thrombotic complications remain one of the most serious and life-threatening conditions that occur in patients with autoimmune diseases, in particular systemic vasculitis. This serves as powerful stimulus for studing the problem of hypercoagulation, which often accompanies the course of systemic vasculitis. Of interest are thrombosis that occure both in the injury of large vessel and in the involvement of medium and small vessels in the pathological process. According to the literature, thrombotic and thromboembolic complications are most common in ANCA-associated vasculitis and Behçet’s disease. This review discusses current studies regarding features of clinical picture and mechanisms of thrombosis development in systemic vasculitis. Because of these studies it became clear that for some vasculitis a high frequency of both arterial and venous thrombosis is characteristic. At the same time, other vasculitis are accompanied by high risk of only venous thrombosis. Finally, thrombosis and thromboembolism are quite rare complications for some vasculitis. Among the presented mechanisms of thrombosis involvement, disruptions of the hemostasis are widely considered. For examples, the presents the results of researches, which is actively discussed the role of neutrophil extracellular traps and antiendothelial cell antibodies in the development on thrombotic complictions. Special attention is paid to the possible role of some disorders of hemostasis, such as polymorphism V coagulation factor G1691FA and prothrombin G20210A. To search for literature sources, the following queries were used: “vasculitis”, “thrombosis”, “neutrophil extracellular traps”, “ANCA-associated vasculitis”, “venous thrombosis”, “arterial thrombosis”, “Behçet’s disease”, “Takayasu arteritis”, “granulomatosis with polyangiitis”, “eosinophilic granulomatosis with polyangiitis”, “Mmicroscopic polyangiitis”, “Henoch–Schönlein purpura”, “Kawasaki disease”, “polyarteritis nodosa”, “giant cell arteritis”, “Buerger’s disease”. In addition, use similar requests in English. The search was carried out in PubMed.

Anti-endothelial cell antibodies in vasculitis: A systematic review.

Anti-endothelial cell antibodies (AECAs) are those that can bind to endothelial cells (ECs) via variable region-specific interactions. The identification and quantification of AECAs varies depending on the technique used. The best approach would be to combine at least two different methods. Thus, AECA measurement cannot be considered a diagnostic tool, but the detection and titers of AECAs are associated with disease activity in various systemic vasculitis diseases. AECAs have been described in almost all primary systemic vasculitis diseases but also in many secondary vasculitis diseases, with the identification of various antigens. AECAs may play a pathogenic role in vasculitis, both in vitro and in vivo, mainly via EC activation and induction of apoptosis. We used a systematic review of the literature to better define the prevalence, clinical association, targeted antigens, possible pathophysiologic role and clinical usefulness of AECAs in various types of vasculitis.

The Level of IgA Antibodies to Endothelial Cells Correlates with Histological Evidence of Disease Activity in Patients with Lupus Nephritis.

Anti-endothelial cell antibodies (AECA) are frequently detected in patients with systemic lupus erythematosus (SLE), but their pathological role remains unclear. We recently developed a solubilized cell surface protein capture enzyme-linked immunosorbent assay (CSP-ELISA) to detect antibodies against membrane proteins involved in autoimmune reactions. In this study, sera from 51 patients with biopsy-proven lupus nephritis (LN), 25 with SLE without renal involvement (non-LN SLE), 42 disease control (DC) subjects, and 80 healthy control (HC) subjects were tested for IgG- and IgA-AECA for human umbilical vein endothelial cells (HUVEC) and human glomerular EC (HGEC) by using CSP-ELISA. IgG- and IgA-AECA titers were significantly higher in LN and non-LN SLE patients than in the DC or HC (P < 0.001) groups. IgG- and IgA-AECA titers for HUVEC corresponded well with those for HGEC. The IgA-AECA level correlated with the SLE disease activity index and with histological evidence of active lesions (cellular proliferations, hyaline thrombi and wire loops, leukocytic infiltration, and fibrinoid necrosis) in LN patients (P < 0.001). The sensitivity of IgA-AECA as a diagnostic test for histological evidence of active lesions in LN patients was 0.92, with a specificity of 0.70. The significant correlation of IgA-AECA with glomerular hypercellularity indicates that IgA-AECA are associated with endothelial damage in LN.

Isolated De Novo Antiendothelial Cell Antibodies and Kidney Transplant Rejection

Studies analyzing the role of antiendothelial cell antibodies (AECAs) in large series of kidney transplant recipients are scarce, and HLA, MHC (major histocompatibility complex) class I-related chain A (MICA), and angiotensin II type 1 receptor have not been formally excluded as targets. Retrospective study of a cohort of kidney transplant recipients. 324 kidney transplant recipients who were negative for anti-HLA, anti-MICA, and anti-angiotensin II type 1 receptor antibodies were tested for AECAs in pre- and posttransplantation serum samples. AECA-positive (preformed [pre+/post+] vs de novo [pre-/post+]) versus AECA-negative (pre-/post-) before or after transplantation. Patient mortality, transplant loss, and acute rejection events. 66 (20%) patients were AECA positive (39 [12%] preformed, 27 [8%] de novo) and 258 (80%) were AECA negative. During a follow-up of 10 years, 7 (18%) AECA pre+/post+ patients had rejections compared with 14 (52%) AECA pre-/post+ and 57 (22%) AECA pre-/post- recipients (OR, 3.80; P=0.001). AECA pre-/post+ status emerged as an independent risk factor for transplant rejection compared to the AECA pre-/post- group (OR, 5.17; P<0.001). However, AECA pre+/post+ and AECA pre-/post+ patients did not show higher risk for either patient death (ORs of 1.49 [P=0.7] and 1.06 [P=0.9], respectively) or transplant loss (ORs of 1.22 and 0.86, respectively; P for both = 0.8) compared to the AECA pre-/post- population. Retrospective study. Posttransplantation sera were collected before or after rejection, entailing a nearly cross-sectional relationship between the exposure and outcome. Lack of identification of precise antigens for AECAs. De novo AECAs may be associated with rejection. These antibodies might serve as biomarkers of endothelium damage in kidney transplant recipients.

Serum anti-endothelial cell antibodies in patients with age-related macular degeneration treated with intravitreal bevacizumab.

To analyse the prevalence and changes in circulating anti-endothelial cell antibodies (AECA) during anti-vascular endothelial growth factor (anti-VEGF) therapy. Ninety-eight patients with exudative age-related macular degeneration (AMD) were treated with intravitreal bevacizumab. Fifty sex- and age-matched healthy subjects were used as controls. Serum AECA were detected using indirect immunofluorescence on primate skeletal muscle and cultivated human umbilical vein endothelial cells (HUVEC). These investigations were repeated at 4-week intervals within 8months of follow-up. At baseline examination, 30 of the 98 patients (30.6%) were positive for AECA. The titres of AECA ranged from 1:10 to 1:320. In the control group, AECA were present in only nine sera (18%) with titres ranging between 1:20 and 1:80 (p=0.0000). The greatest rates of reduction of AECA titres were observed during the 'loading' phase of therapy. During the 'maintenance' phase, the rates of changes in serum AECA levels were less significant and remained constant. In follow-up period in 13 patients (13.3%), serum AECA were detected de novo in titres of 1:10 to 1:80. Statistical analysis did not show any significant correlation between the presence of AECA and activity of the disease. There is growing evidence that AMD is an immune-mediated disease, and thus it cannot be excluded that AECA may be involved in its pathogenesis and progression. We also speculate that AECA develop in response to retinal damage and anti-VEGF therapy.

Anti-Angiotensin II Type 1 Receptor and Anti-Endothelial Cell Antibodies: A Cross-Sectional Analysis of Pathological Findings in Allograft Biopsies.

BackgroundThis is a cross-sectional study designed to evaluate the histologic characteristics of graft injury in the presence of anti-angiotensin II type 1 receptor antibody (AT1R-Ab) and anti-endothelial cell antibody (AECA).MethodsNon-HLA antibody testing was included in the posttransplant evaluation for 70 kidney recipients. Biopsies were performed for cause for 47 patients and as protocol for the remaining 23 patients. Biopsy-proven rejection was defined according to the Banff 2009-2013 criteria. AT1R-Ab was measured on an ELISA platform. Patients were divided into 3 groups based on AT1R-Ab levels (>17, 10-17, and <10 U/ml). AECA was evaluated using an endothelial cell crossmatch (ECXM) in patients whose HLA antibody level was insufficient to cause a positive flow cytometric crossmatch.ResultsAT1R-Ab levels were higher in patients diagnosed with antibody mediated rejection compared to those with no rejection (P = 0.004). Glomerulitis (g) and peritubular capillaritis (ptc) scores were independently correlated with increased AT1R-Ab concentrations in the presence or absence of HLA-DSA (P = 0.007 and 0.03 for g scores; p = 0.005 and 0.03 for ptc scores). Patients with a positive ECXM had higher AT1R-Ab levels compared to those with a negative ECXM (P = 0.005). Microcirculation inflammation (MCI = g + ptc score) was higher in patients with a positive ECXM and with AT1R-Ab >17 U/ml, although this did not reach statistical significance (P = 0.07).ConclusionsThe data show an association between non-HLA antibodies detected in the ECXM and AT1R ELISA and microvascular injury observed in antibody mediated rejection.

Association of Nail Dystrophy With Accrued Damage and Capillaroscopic Abnormalities in Systemic Lupus Erythematosus.

There are some nail abnormalities described in systemic lupus erythematosus (SLE). The aim of this study was to evaluate the association between nail dystrophy (ND) and disease activity, accrued organ damage, capillaroscopic abnormalities, autoantibodies, and some markers of endothelial cell activation in patients with SLE. This was a cross-sectional study of SLE patients from a rheumatology clinic in a tertiary care hospital. Patients were allocated in groups, according to the presence or absence of ND. Demographics, clinical data, disease activity, accrued damage, serology, nailfold capillaroscopy characteristics, serum levels of anti-endothelial cell antibodies, and plasma levels of endothelin 1 were compared between groups. Disease activity was assessed by the Systemic Lupus Erythematosus Disease Activity Index 2000 index and accrued organ damage by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index. Sixty-one patients were included; 50 patients (82%) were female. Thirty-two patients (52.5%) showed ND, and 29 did not. Besides a more frequent use of cyclophosphamide (46.9% vs 20.7%; P = 0.03) in the ND group, clinical features were similar. A greater organ damage was found in patients with ND (median Systemic Lupus International Collaborating Clinics/American College of Rheumatology index = 0.5, minimum = 0, maximum = 6) than in patients without ND (0, 0, 3, respectively; P = 0.04); specifically, only the skin domain was associated with ND (P = 0.04). Onycholysis (40.6%) and longitudinal ridging (25%) were the most frequent nail changes. Nailfold capillaroscopy changes were more frequent in ND patients (40.6%) than in control subjects (13.8%) (P = 0.02). The most frequent nailfold capillaroscopy findings in the ND group were enlarged capillaries (40.6%) and microhemorrhages (12.5%). There was no association between ND and the autoantibody profile, plasma endothelin 1, or serum anti-endothelial cell antibodies. Nail dystrophy was associated with higher accrued organ damage and the presence of capillaroscopic abnormalities. This suggests that ND might be related to chronic microvascular damage.