Additional file 1 of Urinary podocyte stress marker as a prognostic indicator for diabetic kidney disease

Supplementary Material

Patient demographics, clinical characteristics and laboratory parameter results.

<p>Data are mean±SD or median [IQR].</p><p>ERI, EPO Resistance Index, BP, Blood pressure; hsCRP, high sensitivity C Reactive Protein; IL-6, Interleukin 6.</p

The Safety and Short-Term Efficacy of Aliskiren in the Treatment of Immunoglobulin A Nephropathy – A Randomized Cross-Over Study

<div><p>Background</p><p>Laboratory research and previous study suggest that aliskiren, a direct renin inhibitor, has anti-proteinuric effects. We conducted a randomized crossover study to evaluate the anti-proteinuric effect of aliskiren in patients with immunoglobulin A (IgA) nephropathy.</p><p>Methods</p><p>We studied 22 patients with biopsy-proven IgA nephropathy and persistent proteinuria despite angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB). Patients were randomized to either oral aliskiren 300 mg/day or placebo for 16 weeks and then crossed over to the other treatment arm after a washout period. Proteinuria, estimated glomerular filtration rate (eGFR), blood pressure, and serum potassium were monitored.</p><p>Results</p><p>After aliskiren treatment, there was a significant reduction in proteinuria in 4 weeks (1.76±0.95 to 1.03±0.69 g:g-Cr, p<0.0001), which remained at a low level throughout the treatment period. There was a significant difference in proteinuria between the aliskiren and placebo groups from 4 to 16 weeks after treatment (p<0.01 for all comparisons). After aliskiren treatment, there were modest but statistically significant reductions in eGFR (57.2±29.1 to 54.8±29.3 ml/min/1.73 m², p = 0.013) and diastolic blood pressure (72.6±12.3 to 66.2±11.2 mmHg, p<0.0001). None of the patient developed severe hyperkalemia (serum potassium ≥6.0 mmol/l) during the study period.</p><p>Conclusions</p><p>Aliskiren has anti-proteinuric effect in patients with IgA nephropathy and persistent proteinuria despite ACE inhibitor or ARB. Further studies are needed to confirm the renal protecting effect of direct renin inhibition in chronic proteinuric kidney diseases.</p><p>Trial Registration</p><p><a href="http://tinyurl.com/bvez4qn" target="_blank">ClinicalTrials.gov NCT00870493</a></p></div

Multivariable analysis model for natural logarithm of EPO Resistance Index (adjusted for age, albumin, ferritin, PTH and Kt/V).

<p>Multivariable analysis model for natural logarithm of EPO Resistance Index (adjusted for age, albumin, ferritin, PTH and Kt/V).</p

sj-docx-1-tab-10.1177_1759720X221122401 – Supplemental material for High inflammatory burden predicts cardiovascular events in patients with axial spondyloarthritis: a long-term follow-up study

Supplemental material, sj-docx-1-tab-10.1177_1759720X221122401 for High inflammatory burden predicts cardiovascular events in patients with axial spondyloarthritis: a long-term follow-up study by Lin-Hong Shi, Steven H. Lam, Ho So, Edmund K. Li, Tena K. Li, Cheuk-Chun Szeto and Lai-Shan Tam in Therapeutic Advances in Musculoskeletal Disease</p

sj-docx-2-tab-10.1177_1759720X221122401 – Supplemental material for High inflammatory burden predicts cardiovascular events in patients with axial spondyloarthritis: a long-term follow-up study

Supplemental material, sj-docx-2-tab-10.1177_1759720X221122401 for High inflammatory burden predicts cardiovascular events in patients with axial spondyloarthritis: a long-term follow-up study by Lin-Hong Shi, Steven H. Lam, Ho So, Edmund K. Li, Tena K. Li, Cheuk-Chun Szeto and Lai-Shan Tam in Therapeutic Advances in Musculoskeletal Disease</p

Demographic and clinical characteristics of patients with systemic lupus erythematosus.

<p>Values are median (interquartile range, IQR) unless stated otherwise; s.d., standard deviation; n.a., not applicable. SLE, systemic lupus erythematosus; Group 1) Patients with inactive disease (SLEDAI <4) who were never treated with immunosuppressants since the diagnosis or within the past 10 years, whichever longer; Group 2) Patients with inactive disease (SLEDAI <4) who had received or are currently on immunosuppressants; Group 3) Patients with active disease (SLEDAI >4) who had received or are currently on immunosuppressants. SLEDAI, systemic lupus erythematosus disease activity index; SLICC, Systemic Lupus International Collaborating Clinics Score;</p>┼<p>“Never” refers to SLE patients never be given treatment of immunosuppressants [prednisolone, hydroxychloroquine, azathioprine, cyclophosphamide (oral or IV), cyclosporin A and mycophenolate mofetil] since the diagnosis of SLE or within recent 10 years;</p>┼┼<p>“Ever” refer to use of immunosuppressants since the diagnosis of SLE.</p>┼┼┼<p>“<i>Flare</i>” is defined as increase in the SLEDAI score by 3 or more;</p>&<p><i>p</i><0.05,</p>&&<p><i>p</i><0.01,</p>&&&<p><i>p</i><0.001, comparing between Group 1 and Group 2;</p><p>*<i>p</i><0.05,</p><p>**<i>p</i><0.01,</p><p>***<i>p</i><0.001, comparing between Group 1 and Group 3;</p>#<p><i>p</i><0.05,</p>##<p><i>p</i><0.01,</p>###<p>p<0.001, comparing between Group 2 and Group 3.</p

Univariate analysis: the relationship between clinical characteristics, the use of drugs ever and the expression of NOD2 in SLE patients (categorical variables).

┼<p>“<i>Flare</i>” is defined as increase in the SLEDAI score by 3 or more;</p>┼┼<p>“Ever” refers to use of immunosuppressants [prednisolone, hydroxychloroquine, azathioprine, cyclophosphamide (oral or IV), cyclosporin A and mycophenolate mofetil] since the diagnosis of SLE;</p><p>*<i>p</i><0.05.</p

Expression of intracellular NOD2 in CD4⁺ T, CD8⁺ T, CD19⁺ B lymphocytes, monocytes, myeloid dendritic cells and plasmacytoid dendritic cells using flow cytometry.

<p>Group 1) Patients with inactive disease (SLEDAI <4) who were never treated with immunosuppressants since the diagnosis or within the past 10 years, whichever longer; Group 2) Patients with inactive disease (SLEDAI <4) who had received or are currently on immunosuppressants; Group 3) Patients with active disease (SLEDAI >4) who had received or are currently on immunosuppressants. The differential protein expression of intracellular pathogen recognition receptor NOD2 in (A) CD4+ T lymphocytes, (B) CD8+ T lymphocytes, (C) CD19+ B lymphocytes, (D) Monocytes, (E) myeloid dendritic cells (F) plasmacytoid dendritic cells of SLE patients and healthy controls by flow cytometry were shown as median (IQR) of mean fluorescence intensity (MFI) subtracting corresponding isotypic controls in scatter plots.</p

<i>Ex vivo</i> basal production and relative induction of cytokines from NOD2 ligand activated PBMC in various groups.

<p>Culture supernatant was obtained from PBMCs cultured with medium or NOD2 ligand (Muramyl dipeptide, MDP) for 24 hours. The basal production (pg/ml) and relative induction (%) of cytokines (IL-1β, TNF-α, IL-6, IL-8 and IL-10) by PBMCs were analyzed by flow cytometry. Numerical data are expressed as median (interquartile range, IQR). Group 1) Patients with inactive disease (SLEDAI <4) who were never treated with immunosuppressants since the diagnosis or within the past 10 years, whichever longer; Group 2) Patients with inactive disease (SLEDAI <4) who had received or are currently on immunosuppressants; Group 3) Patients with active disease (SLEDAI >4) who had received or are currently on immunosuppressants.</p>&<p><i>p</i><0.05, comparing between Group 1 and Group 2;</p>Δ<p><i>p</i><0.05,</p>ΔΔΔ<p><i>p</i><0.001, comparing between Group 1 with healthy control subjects;</p>Φ<p><i>p</i><0.05,</p>ΦΦ<p><i>p</i><0.01, comparing between Group 2 with healthy control subjects;</p>§<p><i>p</i><0.05,</p>§§<p><i>p</i><0.01 comparing between Group 3 with healthy control subjects.</p