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Proteinuria is a major feature of lupus nephritis (LN) and reflects podocyte injury. Analysis of podocyte biomarkers was performed attempting to identify if podocyte phenotype is distinct in pure membranous and proliferative LN. Expression of synaptopodin, Wilms tumor protein 1 (WT1), glomerular epithelial protein 1 (GLEPP1) and nephrin was evaluated in 52 LN biopsies by immunohistochemistry. Preserved synaptopodin expression was observed in only 10 (19.2%) of all biopsies while 42 (80.8%) had reduced expression. Both groups had comparable proteinuria at the time of biopsy (p = 0.22); however, in the mean follow-up of four years there was a tendency toward lower mean levels of proteinuria in patients with preserved synaptopodin staining (0.26±0.23 vs. 0.84±0.90 g/24 h, p = 0.05) compared with those with diminished expression. Thirty-nine (75%) biopsies were classified as proliferative and 13 (25%) as pure membranous. Comparison of podocyte biomarkers demonstrated a predominance of preserved staining of synaptopodin (69.2%), WT1 (69.2%), GLEPP1 (53.9%) and nephrin (60%) in the pure membranous group whereas only <10% of the proliferative showed preserved expression. Our data suggest that in proliferative forms there seems to occur structural podocyte damage, whereas in the pure membranous the predominant preserved pattern suggests a dysfunctional podocyte lesion that may account for the better long-term prognosis of proteinuria outcome. [ABSTRACT FROM AUTHOR]

Primary antiphospholipid syndrome (PAPS) is associated with increased risk of cardiovascular disease and mortality. Aerobic capacity and cardiac autonomic control are also associated with these risks. The aim of our study was to assess aerobic capacity and cardiac autonomic control in PAPS patients. Thirteen women with PAPS and 13 healthy controls matched for age, gender, and body mass index were enrolled for the study. Both groups were sedentary and were not under chronotropic, antidepressants and hypolipemiant drugs. All subjects performed a treadmill-graded maximal exercise. Aerobic capacity was assessed by peak oxygen uptake (VO2peak), time at anaerobic ventilatory threshold (VAT) and respiratory compensation point (RCP) and time-to-exhaustion, whereas cardiac autonomic control was assessed by chronotropic reserve (CR) and heart rate recovery at the first and second minutes after graded exercise (HRR1min and HRR2min, respectively). All aerobic capacity indexes were reduced more in PAPS patients than in healthy subjects: VO2peak (30.2 ± 4.7 vs 34.6 ± 4.3 ml.kg−1.min−1, p = 0.021), time at VAT (3.0 ± 1.5 vs 5.0 ± 2.0 min, p = 0.016), time at RCP (6.5 ± 2.0 vs 8.0 ± 2.0 min, p = 0.050), time-to-exhaustion (8.5 ± 2.0 vs 11.0 ± 2.5 min, p = 0.010). HRR1min (22 ± 9 vs 30 ± 7 bpm, p = 0.032) and HRR2min (33 ± 9 vs 46 ± 8 bpm, p = 0.002) were delayed in PAPS patients compared to healthy controls but CR was not significantly different (p = 0.272). In conclusion, an impaired aerobic capacity and cardiac autonomic control was identified in PAPS. [ABSTRACT FROM PUBLISHER]

Epidemiological studies with systemic lupus erythematosus (SLE) patients have been reported worldwide but, until now, a large evaluation had not been performed in Brazil. Therefore, we determined the clinical and immunological features of 888 SLE patients followed at our service from 2008 to 2012. The mean age at SLE onset and the mean disease duration were 29.9 ± 9.5 years old and 14.5 ± 8.4 years, respectively. A predominance of female gender (91.9%) and Caucasian ethnicity (69.9%) were observed. Cumulative mucocutaneous manifestations (90.7%) were most commonly identified (malar rash (83.2%), photosensitivity (76.9%)) followed by articular (87.4%), hematological (44.0%) and renal (36.9%) involvements. Antinuclear antibody was detected in all patients, followed by anti-dsDNA (35.1%), anti-Sm (21.8%) and anti-ribosomal P protein antibodies (19.8%). Additional comparison of clinical and laboratory features between genders revealed that malar rash was observed more in female SLE patients (84.5% vs. 69.4%, p = 0.001). Male lupus patients presented a higher frequency of anti-dsDNA (45.8% vs. 34.2%, p = 0.047) and a trend of more nephritis (47.2% vs. 36.0%, p = 0.059). In conclusion, we identified a high prevalence of mucocutaneous manifestations in this Brazilian SLE cohort compared to other countries, mainly malar rash that was most commonly observed in female patients. Anti-dsDNA and other specific SLE autoantibodies were also identified in a higher frequency, predominantly in the male gender. [ABSTRACT FROM AUTHOR]

The influence of antimalarials on lipids in systemic lupus erythematosus (SLE) has been identified in several studies but not in many prospective cohorts. The aim of this study was to longitudinally determine the effect of antimalarials on the lipoprotein profile in SLE. Patients and methods: Fasting total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL) and low-density lipoprotein cholesterol (LDL) plasma levels were determined at entry and after 3 months of hydroxychloroquine (HCQ) treatment in a longitudinal evaluation of 24 patients with SLE. Results: a significant decrease in TC (198 ± 33.7 vs. 183 ± 30.3 mg/dl, p = 0.023) and LDL levels (117 ± 31.3 vs. 101 ± 26.2 mg/dl, p = 0.023) were detected after the 3 months of HCQ therapy. The reduction of 7.6% in TC (p = 0.055) and 13.7% in LDL levels (p = 0.036) determined a significant decrease in the frequency of dyslipidemia (26% vs. 12.5%, p = 0.013) after HCQ therapy. Conclusion: This longitudinal study demonstrated the beneficial effect of antimalarials on lipids in SLE since this therapy induced a reduction of atherogenic lipoproteins. [ABSTRACT FROM AUTHOR]

We compared outcomes of alveolar hemorrhage (AH) in juvenile (JSLE) and adult onset SLE (ASLE). From 263 JSLE and 1522 ASLE, the AH occurred in 13 (4.9%) and 15 (1.0%) patients, respectively (p < .001). Both groups had comparable disease duration (2.6 ± 3.0 vs. 5.6 ± 7.0 years, p = .151) and median SLEDAI scores [17.5 (2 to 32) vs. 17.5 (3 to 28), p = 1.000]. At AH onset, a higher frequency of JSLE were already on a high prednisone dose ( > 0.5 mg/kg/day) compared to ASLE (54% vs. 15%, p = .042). The mean drop of hemoglobin was significantly lower in JSLE (2.9 ± 0.9 vs. 5.5 ± 2.9 g/dL, p = .006). Although treatments with methylprednisolone, plasmapheresis, intravenous immunoglobulin and cyclophosphamide were similar in both groups (p > .050), regarding outcomes, there was a trend in high frequency of mechanical ventilation use (85% vs. 47%, p = .055) and also significant mortality (69% vs. 13%, p = .006) in JSLE compared to ASLE. The sepsis frequency was comparable in both groups (50% vs. 27%, p = .433). We have identified that AH in JSLE has a worse outcome most likely related to respiratory failure. The AH onset in JSLE already treated with high-dose steroids raises the concern of inadequate response to this treatment and reinforces the recommendation of early aggressive alternative therapies in this group of patients. [ABSTRACT FROM AUTHOR]

Objective: To determine the influence of systemic lupus erythematosus (SLE), disease activity, and anticardiolipin antibodies (aCL) on lipid profile, in order to identify patients with high risk for coronary artery disease (CAD).Methods: Fasting lipid profiles were performed in 36 consecutive female SLE patients without any therapy and 30 controls. Exclusion criteria were diabetes mellitus, CAD, liver or thyroid disease, ingestion of lipid-raising drugs, serum creatinine ≥ 1.5 mg/dl, and proteinuria ≥ 0.5 g/d. Disease activity was measured by SLEDAI.Results: High levels of VLDL-C and TG and low levels of HDL-C, the 'lupus pattern', were observed in inactive SLE compared to controls (P < 0.05). Active disease enhanced this difference inducing a more striking increase in VLDL-C and TG levels and also a decrease in HDL-C and LDL-C levels compared to inactive SLE patients (P < 0.05), characterizing the 'active lupus pattern'. Moreover, a significant correlation was found between SLEDAI scores and all lipid fractions. Furthermore these lipid abnormalities were particularly associated with vasculitis. Lower HDL-C levels detected in IgG aCL+ patients compared to IgG aCL - patients were not confirmed by two-way analysis of variance which demonstrated that this difference was exclusively caused by disease activity.Conclusions: Our findings suggest that SLE patients have a lipid profile abnormality which is aggravated by disease activity and may reside in a defect of VLDL metabolism. This pattern of dyslipoproteinemia may increase the risk of developing coronary artery disease. [ABSTRACT FROM PUBLISHER]