nephropathy, including M-type phospholipase A2 receptor (PLA2R), were negative.Electron microscope showed subepithelial electrondense deposits.Based on these findings, a diagnosis of anti-GBM nephritis concurrent with MN was established.Following the addition of fourteen sessions of plasma exchange to the immunosuppressive therapy, the titer of anti-GBM antibody decreased to 4.8 U/mL; however, kidney function failed to recover, and the patient remained dialysis dependent.Conclusion: Discussion: This patient presented with rapidly progressive glomerulonephritis and severe proteinuria.Kidney biopsy demonstrated crescentic anti-GBM glomerulonephritis with MN, based on both linear and granular deposition of IgG and C3 on immunofluorescence and subepithelial electron-dense deposits on electron microscopy.Identification of the specific target antigens (e.g., PLA2R, NELL1, THSD7A, EXT1/2) may confirm primary and secondary MN and assist in guiding appropriate therapeutic approaches.Furthermore, recent reports have shown that MPO immunostaining may be useful in diagnosing MN secondary to MPO-ANCA-associated vasculitis.In this case, we postulated that MN might have preceded and subsequently induced the formation of anti-GBM antibodies.However, these antigen stains were all negative.Nevertheless, these antigen-based analysis provide valuable insight into the underlying pathophysiology.The coexistence of anti-GBM nephritis and MN with MPO-ANCA positivity is exceptionally uncommon, and the clinical relevance of this association warrant further investigation.This work was first presented at ASN Kidney Week 2025, and re-submission is permitted by ASN.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.
Wambugu et al. (Wed,) studied this question.