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Complement Receptor 1 Enhancement in Recurrent Membranous Nephropathy Following Kidney Transplantation: A Case Report
Noriyuki Kounoue1,2, Hideyo Oguchi1, Akinori Hashiguchi3
1Department of Nephrology, Toho University Faculty of Medicine, Tokyo, Japan.
Abstract:
Membranous nephropathy (MN) recurs in some kidney allograft patients, and recurrence increases graft failure rates. We present a unique case of recurrent MN in first and second allografts showing glomerular capillary wall-positivity for complement receptor 1 (CR1) consistent with immunoglobulin G (IgG). A man in his late 20s developed MN and started hemodialysis. MN recurred and caused graft loss after the first transplantation and recurred again soon after the second transplantation. The IgG subclass staining was almost consistently negative for IgG4 and phospholipase A2 receptor (PLA2R)-staining was negative. Recurrent MN of unknown etiology was considered. Mass spectrometry demonstrated that CR1 had increased in the transplanted kidney biopsies. Immunohistochemistry and immunofluorescence studies demonstrated CR1 colocalized with IgG along glomerular capillaries in this case, whereas CR1 was localized in podocytes with no colocalization of IgG in a control case of PLA2R-associated MN. Correlative light and immunoelectron microscopy showed localization of CR1 at the interface between electron-dense deposits and podocytes. Collectively, this case demonstrated a unique enhancement and localization of CR1. MN with enhancement of CR1 has not been reported to date. CR1 may be a candidate causative antigen in this case of recurrent MN, although further study is needed to investigate the pathogenesis of CR1.
Insights
Recurrent membranous nephropathy (MN) in kidney transplants was observed. Complement receptor 1 (CR1) was found to be elevated and colocalized with IgG in glomerular capillaries, suggesting CR1 as a potential antigen in this unique MN case.
Area of Science:
- Nephrology
- Immunology
- Transplantation
Background:
- Membranous nephropathy (MN) recurrence post-kidney transplant leads to increased graft failure.
- Identifying the cause of recurrent MN is crucial for improving patient outcomes.
Observation:
- A unique case of recurrent MN in a patient's first and second kidney allografts is presented.
- Glomerular capillary walls showed positivity for complement receptor 1 (CR1) and immunoglobulin G (IgG).
- Standard markers like IgG4 and phospholipase A2 receptor (PLA2R) were negative.
Findings:
- Mass spectrometry revealed increased CR1 levels in transplanted kidney biopsies.
- Immunohistochemistry and immunofluorescence showed CR1 colocalized with IgG along glomerular capillaries.
- Electron microscopy localized CR1 at the interface between electron-dense deposits and podocytes.
Implications:
- This case highlights a novel finding of CR1 enhancement and specific localization in recurrent MN.
- CR1 is proposed as a potential causative antigen in this form of MN.
- Further research is needed to elucidate the pathogenesis of CR1-associated MN.
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