Clinical and pathological course of recurrent C3 glomerulonephritis from onset to graft loss: a case report

 

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Clinical and pathological course of recurrent C3 glomerulonephritis from onset to graft loss: a case report

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Azusa
Kobayashi
Azusa Kobayashi azusa.0121@gmail.com Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Nephrology Nagoya Japan *
Kenta Futamura kenta88@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Transplant Nephrology and Surgery Nagoya Japan -
Manabu Okada ubanam@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Transplant Nephrology and Surgery Nagoya Japan -
Takahisa Hiramitsu thira@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Transplant Nephrology and Surgery Nagoya Japan -
Hibiki Shinjo shinjo14@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Nephrology Nagoya Japan -
Shoji Saito saito13@med.nagoya-u.ac.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Nephrology Nagoya Japan -
Shunji Narumi nshunji@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Transplant Nephrology and Surgery Nagoya Japan -
Yoshihiko Watarai watarai@nagoya2.jrc.or.jp Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital Transplant Nephrology and Surgery Nagoya Japan -
Asami Takeda a-takeda@masuko.or.jp Masuko Memorial Hospital Nephrology Nagoya Japan -
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Complement 3 glomerulonephritis (C3GN) has a high recurrence rate after kidney transplantation. Before the disease became well understood, kidney transplantation was performed without a diagnosis of C3GN. This report describes a case of recurrent C3GN diagnosed using allograft biopsy and evaluates its long-term clinical and pathological course.


A 35-year-old man with membranoproliferative glomerulonephritis underwent an ABO-compatible living-donor renal transplantation. Three weeks post-transplantation, an allograft biopsy showed prominent granular C3 deposits. One year after transplantation, an allograft biopsy revealed slight mesangial expansion with C3 deposits and a few urinary proteins. Recurrent C3GN was diagnosed based on similar C3 deposition in the native kidney. Eight years post-transplantation, urinary protein levels began to increase and renal function gradually declined. Approximately 10 years after transplantation, an allograft biopsy revealed severe secondary focal segmental glomerulosclerosis and arteriolopathy with no active C3GN lesions. Ten months later, deteriorating kidney function necessitated hemodialysis.

In this case, C3GN recurred early after transplantation, but its activity did not increase for 8 years. The causes of chronic allograft dysfunction vary among cases. More cases and detailed observational studies are needed to determine treatment strategies for recurrent C3GN and graft prognosis.

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