In our case, IL-26 may have potentiated the recruitment of immune cells to the necrotizing lesions through inflammatory cytokines and chemokines, leading to ANCA-associated glomerulonephritis. Anti-GBM disease is caused by autoimmunity to the 3 chain of type IV collagen of GBM. adverse events following mRNA-based COVID-19 vaccination have emerged, such as cases of anti-glomerular basement membrane (GBM) disease or anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) (1,2). The pathogenesis of Butane diacid anti-GBM disease has been well defined at the molecular level, but the factors that initiate the autoimmune process remain unclear (3). AAV is a multisystem autoimmune disease, with neutrophil extracellular traps (NETs) involved in Butane diacid its pathogenesis (4). Interleukin (IL)-26 is a member of the IL-10 family of cytokines that participates in inflammatory signaling through directly binding DNA to facilitate cellular transduction and intracellular inflammation signaling (5). Recently, it has been shown that IL-26 binds to NETs to induce the secretion of inflammatory cytokines (IL-1 and IL-6) and chemokines (IL-8) by myeloid cells in ANCA-associated glomerulonephritis (6). We herein report a case of new-onset anti-GBM disease concomitant with myeloperoxidase (MPO)-ANCA positivity with high levels of serum IL-26 following the receipt of the second dose of the Pfizer-BioNTech COVID-19 vaccine. == Case Report == A 67-year-old man with a history of pulmonary tuberculosis at 25 years old was admitted with a fever and anuria 6 weeks after his second vaccination. He had reported protracted systemic reactions with a low-grade fever and gross hematuria two weeks after the first dose. He received a second dose three weeks after the first dose. One month after the second dose, he developed a fever, anasarca, and anuria, which lasted over the next two weeks. He had received 6 months of chemotherapy for the treatment of pulmonary tuberculosis at 25 years old. There was no history of smoking or medication use, including propylthiouracil. Results of annual medical Butane diacid reviews had been normal, with serum creatinine levels of 0.6 mg/dL and normal urinalysis findings. On admission, his blood pressure was 162/98 mmHg, and a physical examination revealed generalized edema. Laboratory tests revealed a white blood cell (WBC) count of 12,900/mm3, serum creatinine of 14.6 mg/dL, and albumin of 1 1.6 g/dL. A serologic evaluation revealed a C-reactive protein level of 37.0 mg/dL, positive anti-GBM IgG (>3,500 U/mL, reference range 3.0> U/mL), Rabbit polyclonal to ABCA5 positive MPO-ANCA IgG (268 U/mL, reference range 3.5> U/mL), and positive IFN- release assays for tuberculosis. The levels of complement C3 and C4 were within the reference ranges, and testing for proteinase 3-ANCA, anti-nuclear antibody, hepatitis B virus, hepatitis C virus were negative. Polymerase chain reaction and serology testing for severe acute respiratory Butane diacid syndrome coronavirus 2 (SARS-CoV-2) were also negative. A urinalysis revealed blood (3+) and Butane diacid protein (3+) at 4,377 mg/dL, and urine microscopy showed >100 red blood cells per high-power field (>10% dysmorphic) and 100 WBCs per high-power field with granular casts. Computed tomography of the chest revealed nodules in the apex segment of the right upper lobe and bilateral mild pleural effusion, without pulmonary involvement. Three sputum smear examinations with Ziehl-Neelsen staining for the diagnosis of tuberculosis over a three-day period were negative. In addition, there were no negative culture results for those sputum specimens. A kidney biopsy was performed 52 days after the second vaccination. Light microscopy of the kidney biopsy specimen showed cellular crescents and fibrinoid necrosis involving 43 of 45 glomeruli, with CD4 T cells and macrophages scattered throughout the glomeruli. Cortical tubules displayed diffuse acute epithelial injury with interstitial inflammation. Interstitial fibrosis and tubular atrophy were moderate. Immunofluorescence showed linear staining of GBMs for IgG1. Electron microscopy revealed disruption of GBMs and diffuse effacement of podocyte foot processes without immune complex-mediated deposits, leading to a diagnosis of anti-GBM glomerulonephritis (Fig. 1). Further investigations revealed a high serum IL-26 level of 517.1 pg/mL on an enzyme-linked immunosorbent assay (reference range: not detectable), IL-1 of 34.5 pg/mL, IL-6 of 1 1,577.9 pg/mL, tumor necrosis factor- (TNF-) of 300.6 pg/mL, granulocyte colony-stimulating factor (G-CSF) of 126.6 pg/mL, IL-8 of 615.4 pg/mL, and chemokine (C-X-C motif) ligand (CXCL) 1 of.