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Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease and polymorphisms in the cytokine genes and their receptors are thought to influence its development. The aim of this case-control study was to investigate the association of the IL-17A rs2275913, IL-17RC rs708567 and TGFB1 rs1800469 polymorphisms with SLE, its clinical manifestations and the polymorphisms influence on the IL-17A serum levels. Altogether 59 SLE patients with lupus nephritis and 95 healthy controls were genotyped by TaqMan assay. Serum levels were determined by Human IL-17A Platinum ELISA kit. From the studied polymorphisms, only TGFB1 T allele was found to be associated with SLE. Within the patient group, IL-17A GG genotype and TGFB1 -509T allele showed an association with the neurological disease and IL-17RC CC genotype appeared to be associated with lupus arthritis. The IL17A serum levels in the SLE and control groups (7.24 pg/ml and 5.76 pg/ml, respectively) did not show any statistical difference. A weak correlation between IL17A levels and SLEDAI-2K was observed. Our results indicate that IL-17A rs2275913, IL-17RCrs708567 and TGFB1 rs1800469 polymorphisms might play a role in the susceptibility and the clinical manifestations of SLE and IL-17A serum levels should be monitored in the course of the disease. The identification of subsets of SLE with an IL-17-driven disease could improve the therapeutic approach leading to more precise personalized treatment., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

A false-positive result of syphilis screening test (FPST) is a characteristic finding in patients with systemic lupus erythematosus (SLE). We evaluated the clinical characteristics of SLE patients with FPST at SLE diagnosis. We reviewed the medical records of patients with SLE who underwent the Venereal Disease Research Laboratory or Rapid Plasma Reagin tests at SLE diagnosis at Severance Hospital between 2006 and 2016. The baseline characteristics and clinical outcomes were compared between patients with FPST and those with a negative result of syphilis screening test. Of 145 patients with SLE, 20 patients showed FPST and 125 patients showed a negative syphilis screening result. At SLE diagnosis, patients with a negative result had higher SLE disease activity index (5.0 vs. 8.0, P < 0.001) and were more commonly complicated with nephritis (15.0% vs. 41.6%, P = 0.026). High level of serum total protein (> 8 g/dL) and the presence of anti-cardiolipin antibodies were independently associated with FPST (P = 0.010 and 0.037, respectively). During the follow-up (median 61 months), 5 patients with FPST (20.0%) and 12 patients without FPST (9.6%) were finally diagnosed with APS. The long-term risk of de novo thrombosis was higher in the FPST group (n = 4/20, 20% vs n = 6/125, 4.8%, P = 0.041). However, all-cause mortality showed no difference between the FPST group and the negative group. Patients with SLE showing FPST showed lower disease activity at SLE diagnosis but higher thrombotic risk and similar overall survival compared to those without FPST.

Retinopathy in the context of systemic lupus erythematosus (SLE) is associated with severe disease and poorer prognosis. We studied retinopathy in our cohort of Indian lupus patients. Four hundred and thirty-seven patients fulfilling the Systemic Lupus International Collaborating Clinics-American College of Rheumatology-2012 criteria, attending the department of Clinical Immunology were enrolled under this cross-sectional study. A comprehensive clinical (including ophthalmological) examination and immunological profile were performed. Retinopathy was defined if cotton-wool spots, haemorrhages, vasculitis, retinal detachment or optic disc changes as papilledema, optic atrophy were present. Disease activity was assessed using SLE disease activity index (SLEDAI). Mean age of participants was 28.06 ± 9.7 years (93.1% females); median disease duration 12 months (Interquartile range-IQR 6.36). Forty-five (10.3%) had SLE associated retinopathy. Autoimmune haemolytic anaemia [31.1 vs 14.5%, p value 0.004, odd's ratio-OR (95% confidence interval-CI) 2.65 (1.33-5.29)], serositis [33.3 vs 18.9%, p value 0.023, OR (CI) 2.14 (1.11-4.10)], lupus nephritis [62.2 vs 40.8%, p value 0.006, OR (CI) 2.38 (1.26-4.50)], seizures [28.9 vs 12.8%, p value 0.004, OR (CI) 2.77 (1.36-5.65)] and median SLEDAI score (24 vs 12, p < 0.01) were significantly higher in those with retinopathy. On adjusted binary logistic regression, autoimmune hemolytic anemia, lupus nephritis and presence of antibodies to Smith antigen were predictors for retinopathy. Retinopathy is common in SLE, a marker of active disease with frequent renal involvement and should be screened for in all patients with lupus.

There is a pivotal need for new markers to be tested in every day clinical practice for systemic lupus erythematosus (SLE) and lupus nephritis (LN). The levels of monocyte chemoattractant protein-1 (MCP-1) in the serum and urine of 72 SLE patients (27 with LN and 45 without LN involvement) and 30 healthy individuals were studied to establish their clinical significance. The SLE Disease Activity Index (SLEDAI) was used to establish the disease activity. Urine and serum MCP-1 was determined using the sandwich enzyme immunosorbent assay. Urinary, but not serum MCP-1, positively correlated with proteinuria (r = 0.839; p < 0.001) and negatively correlated with glomerular filtration, evaluated using the modification of diet in renal disease (MDRD) formula (r = - 0.293; p < 0.05), and with C3 complement component in active LN patients (r = - 0.519, p = 0.019). Both serum and urinary MCP-1 demonstrated a positive correlation with SLEDAI (r = 0.318; p < 0.01 and r = 0.431; p < 0.001). We also demonstrated that the levels of serum and urinary MCP-1 were significantly higher in patients with SLE compared to healthy controls, regardless of the disease activity and renal involvement. We recommend MCP-1 measurement in the routine laboratory follow-up of the SLE patients.

The aim of this study was to explore whether progranulin (PGRN) can be a useful marker not only for accurate diagnosis of patients with active lupus nephritis (LN), but also for prediction of the disease activity in this population. A total of 154 LN patients were enrolled in this study, 76 of which were diagnosed as having active LN and 78 as having stable LN. Additionally, 71 age-matched non-LN patients were enrolled as controls. The serum and urine PGRN levels of each study population were measured using the enzyme-linked immunosorbent assay method. The diagnostic performance of both indicators and their correlation with the disease activity of LN were systematically investigated using receiver operating characteristic (ROC) analysis and correlation analysis. The active LN population had significantly higher serum and urine PGRN levels than the other two populations. ROC analysis further demonstrated that these two indicators, particularly in combination, appear to have a strong performance in discriminating active LN patients from the rest of the LN population. In the active LN population, serum and urine PGRN levels were not only significantly correlated with SLEDAI score, rSLEDAI score, and activity index, but also had a considerable association with several key markers reflecting the disease activity of LN, including serum levels of complement component 3 and ds-DNA. Nevertheless, neither of the two indicators were correlated with the pathological classification of LN, chronicity index, serum creatinine level, and 24-h urine protein levels. Our findings demonstrate that PGRN may have great potential as a diagnostic factor for active LN and as a predictor for its disease activity.

Current management guidelines for lupus nephritis (LN) do not attach importance to histological indices of disease activity or chronicity. The present study was performed to evaluate the clinical relevance of these indices in determining outcomes in patients with class IV LN. We analyzed the data of all patients with biopsy-proven class IV LN seen over a 6-year period. The histopathological findings were reviewed; the activity and chronicity indices proposed by Austin [AI (Austin) & CI (Austin)] and the renal biopsy index proposed by Hill were calculated. As immunofluorescence was not done in all patients, this was excluded from calculation of the renal biopsy index, which was referred to as the modified Hill's index (MHI), which was a composite of glomerular activity index (GAI), chronicity index (CI) and tubulo-interstitial activity index (TIAI). Pearson's correlation coefficient, multilinear regression analysis and logistic analysis were performed, and p value of <.05 was considered significant. During the study period, 114 cases of LN were evaluated, of which 64 % (73/114) had class IV LN. The mean age was 26.5 years, and 92 % were females. The mean scores of AI (Austin), CI (Austin), GAI, CI, TIAI and MHI were 8.46, 2.50, 7.54, 3.06, 4.74 and 2.23, respectively. Serum creatinine correlated significantly with TIAI, CI, CI (Austin) as well as MHI, but not with AI (Austin) or GAI. The serum creatinine level was the strongest clinical parameter determining outcome, while none of the histological indices correlated with either treatment outcome or mortality. None of the histological indices performed better than serum creatinine level in determining the treatment outcomes and mortality.

Anti-P antibodies have been associated with organ involvement in SLE, such as in autoimmune hepatitis, and have been suggested to be directly pathogenic. Neuropsychiatric lupus, lupoid hepatitis, autoimmune hepatitis, lupus nephritis, and Chagas' disease have been associated with the presence of anti-P antibody. This review seeks to look into the current literature on anti-P antibody and the association between SLE and non-SLE autoimmune connective tissue disorder.

Growth arrest-specific protein 6 (Gas6) is a serum protein involved in granulocyte, platelet and endothelium interaction, and is implicated in both anti-inflammatory response as well as platelet/leukocytes activation. We investigated serum Gas6 level in different clinical manifestations of systemic lupus erythematosus (SLE). Data were collected in 83 patients with SLE and 40 non-lupus controls. The Gas6 levels were detected by enzyme-linked immunosorbent assay. Our results demonstrated that the Gas6 level was higher in SLE patients as compared to the non-lupus control subjects (SLE vs. non-lupus control, median [inter-quartile range (IQR)] 22.67 [19.40-28.60] vs. 18.97 [16.05-20.62] ng/mL, p < 0.01). Furthermore, Gas6 level was higher in patients with nephritis (nephritis vs. non-nephritis, median [IQR] 26.21 [21.17-31.61] vs. 22.22 [18.98-26.98] ng/mL, p = 0.03) and in patients with cutaneous vasculitis (vasculitis vs. non-vasculitis, median [IQR] 27.89 [23.24-34.26] vs. 22.30 [19.32-27.16] ng/mL, p = 0.03). Our results indicate that the serum Gas6 level is increased in SLE patients with lupus nephritis or cutaneous vasculitis, implicating a potential to serve as a SLE disease activity marker.

Data about clinical-laboratory features and outcome of antiphospholipid syndrome nephropathy (APSN) in the course of lupus nephritis (LN) are scarce. To determine prevalence, clinical correlations and outcome of APSN in patients with LN, retrospective analysis of renal specimens and review of medical records from 48 LN patients were performed. APSN was found in 12/48 (25 %) of LN. Positivity for lupus anticoagulant (LAC) and double antiphospholipids positivity [LAC plus anticardiolipin (aCL)] were significantly more frequent in APSN-LN (p = 0.02 and p = 0.01, respectively) than in LN, while single aCL positivity was not. Overt antiphospholipid syndrome appeared more frequent in patients with APSN-LN (p = 0.05). There were no statistically significant differences between APSN-LN and LN in the proportion of each World Health Organization class of LN (with the exception of a trend toward fewer Class III LN in APS-LN) and in the systemic lupus erythematosus (SLE) disease duration and severity. At the time of renal biopsy, patients with APSN-LN had median serum creatinine levels significantly higher than patients with LN [1.45 (0.6-6.6) vs. 1.00 (0.7-3.0), p = 0.02]. Double antiphospholipid positivity was the only variable significantly associated with APSN-LN at multivariate regression analysis (OR 8, 95 % CI 1.7-37, p = 0,008). APSN-LN and LN did not differ significantly as regards the rate of complete (25 vs. 19.4 %, p = 0.72) and partial treatment response (25 vs. 29 %, p = 0.82) at 6 months and the progression to end-stage renal disease after a median follow-up of 8.1 ± 3.6 years (16.6 vs. 13.8 %, p = 0.82). APSN was demonstrated in a quart of LN, appeared to be independent from underlying LN class and SLE severity, and did not seem to confer a worse prognosis to LN. The findings of higher creatinine and more interstitial fibrosis in APSN should be confirmed in future prospective larger studies.

Systemic lupus erythematosus (SLE) is a prototype autoimmune disease characterized by systemic inflammation and autoantibody production. Anti-mannose binding lectin (anti-MBL) autoantibodies have been studied in SLE for their possible effect on mannose binding lectin (MBL) levels and functional activity. This study aimed at the detection of anti-MBL autoantibodies in Indian SLE patients and evaluates their relationship with related immunological parameters. Two hundred diagnosed SLE patients from Western India were included in the study where 87 patients were lupus nephritis (LN) (43.5 %) and remaining (56.5 %) were non-LN. Disease activity was assessed using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Anti-MBL autoantibodies to IgG and IgM isotypes, anti-C1q autoantibodies, MBL levels and circulating immune complex levels were detected by ELISA. C3, C4 and CRP levels were detected by nephelometer. Anti-MBL autoantibodies were detected in 52 % SLE patients, where 55 % had IgG-anti-MBL, 33.8 % had IgM-anti-MBL and 11.3 % had both subclasses. Low MBL levels were present in 64.4 % anti-MBL positives as compared to 61.5 % in anti-MBL negatives. Among anti-MBL positives, 74 % had anti-C1q antibodies, whereas 41.7 % of anti-MBL negatives had anti-C1q autoantibodies (p = 3.45E06). An inverse correlation was observed between serum MBL and CIC levels. A statistically significant difference was noted between anti-MBL positives and anti-MBL negative patients with hsCRP levels (p = 0.002). Occurrence of infections was higher among anti-MBL positives (65 %) as compared to anti-MBL negatives (35 %). The difference between SLEDAI scores among anti-MBL-positive and anti-MBL-negative groups was statistically insignificant. Anti-MBL autoantibodies in SLE patients can influence functional activity of MBL and have a significant role in SLE disease pathogenesis.

Associations of different assays for antibodies to C1q (anti-C1q) and to dsDNA (anti-dsDNA) and of complements C3 and C4 with disease activity in patients with systemic lupus erythematosus (SLE) were studied. The clinical manifestations of 223 SLE patients were recorded, and the disease activity was assessed by the SLEDAI score. Anti-C1q were determined by two enzyme-linked immunosorbent assays (ELISA) and anti-dsDNA by a radioimmunoassay (RIA), a Crithidia immunofluorescence (IF) assay and three ELISA assays using human telomere DNA, plasmid DNA circles, or calf thymus DNA as antigens, respectively. Complement C3 and C4 were determined by nephelometry. Control sera were obtained from 98 blood donors. In patients with SLE, the prevalence of anti-C1q was 17-18% and that of anti-dsDNA was 36-69%. Anti-C1q, anti-dsDNA, and complement C3 and C4 correlated well with the overall activity of SLE (r = 0.323-0.351, 0.353-0.566, and -0.372-0.444, respectively; P < 0.001). Sensitivity, specificity, positive predictive value, and negative predictive value for active lupus nephritis among SLE patients were 40-44, 92, 29, and 91-92% for anti-C1q and 48-68, 29-66, 11-16, and 86-91% for anti-dsDNA, respectively. Patients with active nephritis had higher levels of anti-C1q and lower levels of C3 and C4 than patients with inactive nephritis (P = 0.003-0.018). The corresponding associations of anti-dsDNA were somewhat weaker (P = 0.023-0.198). Hematological parameters reflecting disease activity correlated clearly better with anti-dsDNA and complement C3 and C4 than with anti-C1q. Anti-C1q is inferior to anti-dsDNA as a diagnostic test in SLE and in the evaluation of overall clinical activity of the disease. Anti-C1q together with complement C3 and C4 may offer useful additional information to monitor lupus nephritis activity. There are no practical differences between different assays for anti-C1q and anti-dsDNA.

Few studies have evaluated the glomerular filtration rate (GFR) in patients with systemic lupus erythematosus (SLE). Even though the National Kidney Foundation (NKF) suggests using the equations to estimate GFR, rheumatologists continue using creatinine clearance (CCl). The main objective of our study was the assessment of different equations to estimate GFR in patients with SLE: Simplified MDRD study equation (sMDRD), CCl, Cockcroft Gault (CG), CG calculated with ideal weight (CGi), Mayo Clinic Quadratic (MCQ), and Chronic Kidney Disease Epidemiology Collaboration Equation (CKD-EPI). CKD-EPI was considered as the reference standard, and it was compared with the other equations to evaluate bias, correlation (r), sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), percentage of measurement of GFR between 70-130% of GFR measured through CKD-EPI (P30) and to compute the ROC curves. Adequacy of the 24-h urine collection was evaluated. To classify patients into GFR < 60 ml/min/1.73 m(2), the best sensitivity and NVP were obtained with sMDRD: the best PPV and specificity with MCQ. P30 was 99.3% with sMDRD, 77.5% CCl, 91.7% CG, 96.7% CGi, and 77.2% with MCQ. The lowest bias was for sMDRD and the highest for CCl. Only 159 (52.6%) urine collections were considered adequate, and when these patients were re-evaluated, the statistical results improved for CCl. CGi was better in general than CG. CCl should not be considered as an adequate GFR estimation. Ideal weight is better than real weight to calculate GFR through CG in patients with SLE.

The aim of the present study is to assess the association of elevated serum uric acid (UA) with lupus nephritis (LN) in systemic lupus erythematosus (SLE) patients. A total of 130 SLE patients were recruited, of whom 73 patients developed LN. Blood samples were obtained for determination of uric acid, complement 3 (C3), C-reactive protein (CRP) and some autoantibodies including anti-double-stranded DNA, -Smith, -SSA, -SSB, -U1RNP, SCL-70, and -Jo-1 antibodies. Correlations of UA with LN were assessed. UA was an independent risk factor for LN [odds ratio (95% CI): 1.01 (1.005-1.014); P=0.0000]. The best cut-off value for UA using the ROC curve was 330 μmol/L (sensitivity 78.1% and specificity 75.4%) and the area under the ROC curve was 0.803±0.039 (95% CI: 0.727-0.878, P=0.000). Spearman's correlation coefficient analysis showed negative association of UA with C3 in SLE patients with LN (r=-0.356, P=0.002), but no association in those without LN. No correlations were found between UA and age, SLEDAI, CRP, IgG, IgM or IgA. Furthermore, analysis of covariance demonstrated that anti-Sm (β=-0.218, P=0.004) and -U1RNP (β=0.177, P=0.008) autoantibodies were independent determinants of serum UA. The UA level is independently associated with the development of LN in SLE patients.

The objective of the study is to determine whether the activity of DNase1 is associated to the presence of nephropathy in patients with SLE. Forty-five patients affected with SLE and renal involvement were analyzed. The type of renal involvement was type III or IV glomerulonephritis. At least two serum samples were withdrawn from each patient, one obtained in a renal flare and the other obtained in a period of clinical stability. C3 and C4 complement levels and anti-DNA antibodies were determined. DNase1 activity was measured using a radial enzyme-diffusion method. Results suggest that when comparison of DNase1 activity was established between samples obtained during a phase of active renal involvement and those obtained in the clinically stable phase, we did not find statistically significant differences. When the comparison was performed with matched samples of the same patient, DNase1 activity was lower when patients had active renal involvement than when samples were taken in clinically stable phase (21.21 μg/ml ± 16.47 vs. 25.62 μg/ml ± 18.81, p < 0.05). No difference in DNase1 activity was observed between samples positive or negative for anti-DNA antibodies. No difference in DNase1 activity was found in patients with normal or decreased levels of C3 (25.09 μg/ml ± 17.78 vs. 20.01 μg/ml ± 16.15, p = 0.073) or C4 (23.52 μm/ml ± 16.60 vs. 19.62 μg/ml ± 17.54, p = 0.060). We conclude that low DNase1 activity is associated to the active phase of type III or IV nephropathy. Therefore, it is possible that this enzyme plays an important role in the development of SLE nephropathy.

Gender may produce different characteristics in the manifestation of systemic lupus erythematosus (SLE). The present study investigated the influence of gender on clinical, laboratory, autoantibodies and histopathological classes of lupus nephritis (LN). As much as 81 patients diagnosed with SLE (ACR criteria) and active nephritis, who underwent renal biopsy between 1999 and 2004, and who had frozen serum samples and clinical data available from the time of biopsy, were selected for this study. The presence of anti-P and antichromatin antibodies was measured using ELISA, and anti-dsDNA was measured using indirect immunofluorescence. All of the renal biopsies were reviewed in a blinded manner by the same expert renal pathologist. The charts were extensively reviewed for demographic and renal features obtained at the time of the biopsy. Of the 81 patients (13.6%), 11 were male SLE patients. Both male and female lupus patients were of similar age and race, and had similar durations of lupus and renal disease. The female patients had more cutaneous (95.7 vs. 45.5%, P = 0.0001) and haematological (52.9 vs. 18.2%, P = 0.04) involvements than the male SLE patients. In addition, the articular data, central nervous system analyses, serositis findings and SLEDAI scores were similar in both experimental groups. Positivity for anti-dsDNA, anti-ribosomal P and antichromatin did not differ between the two groups, and both groups showed similarly low C3 or C4 serum levels. Our analysis indicated that no histopathological class of LN was predominant in both males and females. Interestingly, the serum creatinine levels were higher in the male SLE patients compared to the female SLE group (3.16 +/- 2.49 vs. 1.99 +/- 1.54 mg/dL, P = 0.03), with an increased frequency of high creatinine (81.8 vs. 47.1%, P = 0.04) as well as renal activity index (7.6 +/- 3.5 vs. 4.8 +/- 3.5, P = 0.02). In addition, whilst the mean levels of proteinuria, cylindruria and serum albumin were markedly altered, they were comparable between both lupus men and women. Moreover, the frequencies of dialysis, renal transplantation and death were similar between the two groups. These data suggest that male patients had a more severe LN compared to women diagnosed with this renal abnormality.

Recent evidence suggests that matrix metalloproteinases (MMPs) were involved with many kinds of kidney diseases. We investigated the roles of MMPs and its tissue inhibitors TIMPs in patients with lupus nephritis (LN). A total of 44 systemic lupus erythematosus patients and 31 healthy subjects were enrolled. The levels of total MMP-2, 9 (tMMP-2, tMMP-9) along with TIMP-1, 2 were measured in serum by ELISA. Serum tMMP-2, tMMP-9 was higher in LN patients than those non-LN patients and healthy controls. Serum tMMP-2 in patients without LN was higher than in healthy controls. TIMP-2 was higher in LN patients than healthy controls, and no significant difference in TIMP-2 was observed between LN and non-LN patients. TIMP-1 levels among LN, non-LN patients and healthy controls were comparable. The ratio of tMMP-9 to TIMP-1 in LN patients was higher than non-LN patients and healthy controls and no difference in ratio of tMMP-9 to TIMP-1 between non-LN patients and healthy subjects was observed. A negative correlation between the ratio of tMMP-9 to TIMP-1 in lupus patients and the titers of anti-dsDNA was found; whereas, no correlation between the ratio of tMMP-9 to TIMP-1 and the concentration of C3 as well 24 h urine protein was observed in LN patients. We suggest imbalance between tMMP-9 and TIMP-1 may contribute to the pathogenesis of LN. Measurement of MMPs and TIMPs may be helpful in the early identification of lupus patients with LN and may help gauge the response to treatment in patients with active LN undergoing treatment.

Twenty-five children (20 girls and five boys) with lupus nephritis seen over last 12 years, were evaluated. Twenty underwent renal biopsies. Cyclophosphamide pulse therapy was used in eight patients (median 14 pulses, range 6-16) with severe disease or histological class. Four of these eight patients became asymptomatic (class IV, 2; class II and V, one each) after 4-24 months. Two (class III and IV, one each) died after a stable chronic renal insufficiency for almost a decade; one died 9 months after diagnosis (class IV). Of the 12 patients who underwent biopsy but were not treated with cyclophosphamide, six became asymptomatic during follow up (class II, four patients; class VI and V, one each), two continued to have proteinuria (class II), one (class IV) had raised ESR but normal renal functions and two died (class IV). Three of the five patients who were not biopsied remained asymptomatic; two were lost to follow up. Mortality was seen only with class III (one patient) or class IV (five patients) lesions. Outcome in lupus nephritis depends largely on WHO histological class. Cyclophosphamide pulse therapy is associated with a favorable outcome.

We analysed the frequency of autoantibodies in 44 patients with lupus nephritis. Antinuclear antibody (ANA) was found in 91% of patients by an indirect immunofluorescence technique on HEp-2 cells at the time of study. Anti-dsDNA antibodies were found at high levels in most of the patients using the SynELISA test, which reveals both high and low avidity antibodies, but only in 64% of patients using the DAKO assay, which reveals high avidity antibodies. Anti-histone antibodies were found in 52% of the patients. Anti-SSA/Ro antibodies were positive in 27% of all patients; these patients also had prominent cutaneous involvement and photosensitivity. The frequency of anti-SSB/La and Anti-Sm antibodies was 7%. Immunoblotting experiments confirmed the findings shown by the techniques described above, and anti-ribosomal antibodies were found to be positive in more cases by the latter assay. IgA rheumatoid factor (RF) was more frequent (20.4%) than IgM RF (9.9%). In conclusion, Turkish patients suffering from lupus nephritis seem to express a total autoantibody profile similar to that reported for systemic lupus erythematosus from other parts of Europe.

A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. The MRL/lpr/lpr mouse is an established model for SLE, developing both antinuclear and anti-type II collagen autoantibodies, and rheumatoid factors(s), exhibiting reduced complement levels and later on developing glomerulonephritis and often arthritis. We report here an age-dependent decrease in serum C1q levels coincident with the development of IgG2b autoantibodies reactive with mouse C1q in MRL/lpr/lpr mice. Unlike IgG2b, although high levels of IgM, IgG1 and IgG2a are present in these mice, few, if any, antibodies of these subclasses reactive with mouse C1q were observed in this study. This is the first report of autoantibodies against autologous C1q in an animal model, and the results should facilitate in clarification of the roles of C1q and autoantibodies reactive with C1q in SLE, as well as their potential connection with glomerulonephritis.

As autoantibodies are thought to participate in the pathogenesis of renal inflammation in systemic lupus erythematosis (SLE) we investigated associations between serological markers of disease activity in SLE and the activity of renal histopathological lesions in thirty-five patients with lupus nephritis (LN). We found the following prevalence of serum auto-antibodies in LN: IgG antinuclear antibodies (ANA) 100%, IgM ANA 69%, IgA ANA 60%, IgG anti-dsDNA 60%, IgM anti-dsDNA 71%, IgA anti-dsDNA 60%, anti-RNP 20%, anti-Sm 14%, anti-SSA 31%, anti-SSB 14%, anti-histone 37%, anti-cardiolipin 80% and antibody to ribosomal protein (anti-P) 6%. No correlation was found between serological parameters and the WHO-classification of biopsies. The activity-index of histological lesion, assessed according to the NIH-renal histology scoring system, correlated with IgM ANA and IgM anti-dsDNA titers. Of all the specific features of histological renal inflammation, glomerular proliferation showed the best overall correlation with serological parameters of disease activity. Anticardiolipin antibodies were correlated with overall disease activity, but not with renal histological activity. Thus, serological markers of disease activity did not adequately reflect the amount of renal inflammation in LN and cannot replace renal biopsy as a diagnostic tool.