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Recurrent C3 Glomerulonephritis along with BK-Virus-Associated Nephropathy after Kidney Transplantation: A Case
Jeong-Hoon Lim1, Seong-Won Shin1, Mee-Seon Kim2
1Department of Internal Medicine, School of Medicine, Kyungpook National University Hospital, Kyungpook National University, Daegu 41944, Republic of Korea.
Insights
C3 glomerulonephritis (C3GN) often recurs after kidney transplantation (KT). Managing C3GN recurrence with immunosuppression may increase the risk of BK-virus-associated nephropathy (BKVAN) in kidney transplant recipients.
Area of Science:
- Nephrology
- Transplantation Immunology
Background:
- C3 glomerulonephritis (C3GN) is a rare cause of end-stage kidney disease.
- C3GN frequently recurs in kidney allografts post-transplantation.
Observation:
- A kidney transplant recipient developed recurrent C3GN and BK-virus-associated nephropathy (BKVAN).
- Recurrent C3GN was treated with increased immunosuppression, leading to normal C3 levels.
- Subsequent increase in BK viral load and graft dysfunction prompted a decrease in immunosuppression, improving BKVAN.
Findings:
- C3GN recurrence post-kidney transplantation is common.
- Immunosuppressive therapy for C3GN recurrence can increase the risk of BKVAN.
Implications:
- Careful monitoring and adjustment of immunosuppression are crucial in kidney transplant recipients with C3GN.
- This case highlights the complex interplay between C3GN recurrence and BKVAN in kidney allografts.
Abstract:
C3 glomerulonephritis (C3GN) is a rare cause of end-stage kidney disease and frequently recurrent in allografts following kidney transplantation (KT). Herein, we describe the case of a kidney transplant recipient who developed recurrent C3GN along with BK-virus-associated nephropathy (BKVAN) following KT. A 33-year-old man diagnosed with membranoproliferative glomerulonephritis 17 years ago underwent preemptive KT with a donor kidney from his aunt. Proteinuria gradually increased after 3 months following KT, and graft biopsy was performed 30 months after KT. Histopathological examination revealed recurrent C3GN. The dosages of triple immunosuppressive maintenance therapy agents were increased. Subsequently, serum C3 levels recovered to normal levels. However, at 33 months following KT, the BK viral load increased and graft function gradually deteriorated; a second graft biopsy was performed at 46 months following KT, which revealed BKVAN and decreased C3GN activity. The dosages of immunosuppressive agents were decreased; subsequently, BKVAN improved and graft function was maintained with normal serum C3 levels at 49 months following KT. This case indicates that C3GN is highly prone to recurrence following KT and that immunosuppressive therapy for C3GN increases the risk of BKVAN.
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