Aim To assess association between urinary levels of adiponectin and severity of renal involvement in SLE patients. Also, this study aims to determine the value of urinary adiponectin levels to discriminate renal involvement in these patients. Methods In a multi‐center cross‐sectional survey, 50 consecutive patients diagnosed as having systemic lupus erythematosus (SLE) according to American College of Rheumatology criteria were classified into two groups with or without renal involvement (microscopic hematuria, reduced glomerular filtration rate < 25% of normal value, and proteinuria > 500 mg/24 h) which was confirmed by renal biopsy. Urinary adiponectin was measured by enzyme‐linked immunosorbent assay. SLE disease activity levels were assessed by SLE Disease Activity Index (SLEDAI) score. Results Comparing urinary levels of adiponectin between the two groups indicated considerable discrepancy in this index between the groups with and without renal involvement (146.33 ± 258.83 ng/mL vs. 22.96 ± 44.33 ng/mL, P = 0.023). Also, urinary adiponectin/creatinine ratio was significantly higher in the former group (221.72 ± 414.58 vs. 19.99 ± 41.19, P = 0.019). Our study showed a higher mean SLEDAI score in those with renal involvement than others (23.60 ± 2.53 vs. 9.12 ± 3.03, P < 0.001). Multivariable linear regression analysis with the presence of potential confounders showed that the level of urinary adiponectin was significantly higher in those with renal involvement than other patients (β = 0.470, P = 0.023). The optimal cut‐off point for urinary adiponectin levels to discriminate renal involvement from normal renal state was 7.5 ng/mL, yielding a sensitivity of 80% and specificity of 52%. Conclusion Urinary levels of adiponectin are significantly elevated in SLE patients with renal involvement. The measurement of this biomarker can be helpful to discriminate impaired from normal renal function in SLE patients.

Background Severe acute respiratory syndrome coronavirus 2 may be associated with late-onset necrotizing myositis, mimicking autoimmune inflammatory myositis; however, the exact underlying pathogenesis of severe acute respiratory syndrome coronavirus 2-induced myositis is still unclear. Case Presentation Herein, we report a rare case of necrotizing autoimmune myositis in a 67-year-old middle eastern male following coronavirus disease 2019 infection, who presented with muscle weakness. The patient had positive anti-NXP2. The diagnosis of necrotizing autoimmune myositis was made according to muscle weakness, increased liver enzymes, electromyography and nerve conduction velocity results, and muscle biopsy. The patient underwent a full malignancy evaluation, which was unremarkable, and was discharged in relatively well condition with a daily dose of 1 mg/kg prednisolone and azathioprine 150 mg (2 mg/kg). Conclusion Our report highlights the already known possible protracted sequence of coronavirus disease 2019 infection and the potential for delayed-onset necrotizing myositis.

Background Antineutrophil cytoplasmic antibody-associated vasculitis is dominated by inflammatory occlusion of small vessels, causing tissue ischemia in various organs. This disorder has rarely been associated with vasculopathy, such as antiphospholipid syndrome. Case presentation We report a case of a 48-year-old Persian male presenting with distal digital gangrene along with inflammatory arthralgia. High titers of anti-proteinase 3 and antiphospholipid antibodies (anticardiolipin antibody) were detected in laboratory evaluation. Therefore, a diagnosis of antineutrophil cytoplasmic antibody-associated vasculitis and antiphospholipid syndrome was made and treated with anticoagulant along with monthly pulses of cyclophosphamide and a daily dose of 1 mg/kg prednisolone. Conclusion Our case, along with other reports, illustrates that these two entities can coexist. Therefore, monitoring antiphospholipid antibodies in patients with antineutrophil cytoplasmic antibody-associated vasculitis with or without clinical evidence of any thrombosis and ruling out thrombosis in cases that do not respond to proper treatment of vasculitis may be relevant to prevent irreversible or fatal organ damage.