Antiphospholipid antibody positivity and levels.

<p>Antiphospholipid antibody positivity and levels.</p

Comparisons with regard to clinical response to induction treatment.

<p>Comparisons with regard to clinical response to induction treatment.</p

Patient characteristics.

<p>Patient characteristics.</p

Comparisons with regard to the induction treatment regimen.

<p>Comparisons with regard to the induction treatment regimen.</p

Comparisons between baseline and post-treatment outcomes.

<p>Comparisons between baseline and post-treatment outcomes.</p

Creatinine levels (μmol/L) in LN patients with and without IgG aPL.

<p>At baseline, creatinine levels were higher in LN patients with (n = 8) versus without (n = 56) IgG aCL (A; median: 104.5 μmol/L, range: 64–185, versus 77.0 μmol/L, range: 46–284; p = 0.03). Consistently, creatinine levels were higher in LN patients with (n = 9) versus without (n = 55) IgG anti-β₂-GPI (B; median: 94.0 μmol/L, range: 64–18, versus 75.0 μmol/L, range: 46–284; p = 0.02). Similar findings were observed post-treatment, with higher creatinine levels in LN patients with (n = 6) versus without (n = 58) IgG aCL (C; median: 86.5 μmol/L, range: 72–128, versus 75.5 μmol/L, range: 40–306; p = 0.04), as well as with (n = 6) versus without (n = 58) IgG anti-β₂-GPI (D; median: 86.5 μmol/L, range: 72–128, versus 75.5 μmol/L, range: 40–306; p = 0.04). Bounds of the boxes denote the 25^th and 75^th percentiles (IQR). Lines in the boxes denote the 50^th percentile (median). Whiskers denote the range. Circles (out values, 1.5–3 IQRs further from the closest box bound) and stars (far out or extreme values, ≥3 IQRs further from the closest box bound) denote outliers. Some extreme values do not appear in the figure due to scaling. LN: lupus nephritis; aCL: anticardiolipin antibodies; anti-β₂-GPI: anti-β₂-glycoprotein I antibodies.</p

Association of 5676 SNPs to lupus nephritis in case-control analysis of 195 patients.

<p>Results from the association analysis of 5676 SNPs in 195 patients with lupus nephritis and 512 healthy controls in cohort I. The negative logarithm of the p-value is plotted against the chromosomal location. The line represent associations with p<0.001 and the nine genes associated with p<0.001 are indicated. The <i>STAT4</i> SNPs rs11889341, rs7574865, rs7568275 and rs7582694 have an r² = 0.98 calculated from the 512 controls.</p

Case-control association analysis in cohort I^a. The best SNPs in genes associated with lupus nephritis with p <0.001 are shown.

<p>The best SNP in each gene is shown and for STAT4, IRF5, TNIP1 and BLK also the SNPs used for meta-analysis, marked in bold; STAT4 rs11889341, rs7582694 r² = 0.98, IRF5 rs2070197, rs10488631 r²≈1.00, TNIP1 rs7708392, rs6889239 r²≈1.00 and BLK rs922483, rs13277113 r² = 0.87 calculated in 512 Swedish controls. OR: odds ratio, CI: confidence interval, NA: not available.</p><p>^a Uppsala, Stockholm and Lund, Sweden, n = 567 SLE cases, n = 512 controls</p><p>^b WHO class III or IV on renal biopsy, according to the 1995 WHO classification system <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-Churg1" target="_blank">[2]</a>.</p><p>^c Glomerular filtration rate <30 mL/min/1.73 m²<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-KDOQI1" target="_blank">[22]</a>.</p><p>^d rs3135394 has an r² = 0.87 with the HLA*DR3 (DRB1*0301) allele <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-Gateva1" target="_blank">[6]</a>.</p><p>^e Unadjusted p-value and OR for differences in allele frequencies between patients and controls.</p><p>^f Adjusted p-value and OR from logistic regression analysis including age and gender as covariates. Number of cases and controls; lupus nephritis, n = 194, proliferative nephritis, n = 91, severe renal insufficiency, n = 28, SLE, n = 566, controls, n = 504.</p

Case-control meta-analysis of cohort I^a and cohort II^b in a total of 712 SLE cases and 1131 controls.

<p>^a Uppsala, Stockholm, Lund, n = 567 cases, n = 512 controls.</p><p>^b Linköping, n = 145 cases, n = 619 controls.</p><p>^c WHO class III or IV on renal biopsy, according to the 1995 WHO classification system <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-Churg1" target="_blank">[2]</a>. Biopsies available in 178 patients.</p><p>^d Glomerular filtration rate <30 mL/min/1.73 m²<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-KDOQI1" target="_blank">[22]</a>. Data available for 225 patients.</p><p>^e Unadjusted combined p-value and OR calculated using Cochran-Mantel Haenszel chi-square test. P-values remaining significant after Bonferroni correction for 4 tested SNPs are in italic.</p><p>^f Adjusted p-value and OR from meta-analysis of logistic regression results including age and gender as covariates. Number of cases and controls; lupus nephritis, n = 229, proliferative nephritis, n = 111, severe renal insufficiency, n = 31, SLE, n = 711, controls, n = 960.</p

Patient basic characteristics.

<p>^a Uppsala, Stockholm and Lund, Sweden</p><p>^b Linköping, Sweden</p><p>^c Comparison between SLE with lupus nephritis and SLE without lupus nephritis. Frequencies compared with Chi square test and continuous variables with Mann-Whitney U-test.</p><p>^d WHO class III or IV on renal biopsy, according to the 1995 WHO classification system <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-Churg1" target="_blank">[2]</a>. Biopsy data was not available from all patients.</p><p>^e Glomerular filtration rate <30 mL/min/1.73 m²<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084450#pone.0084450-KDOQI1" target="_blank">[22]</a>.</p