ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: FR-PO743

Infection: A Potential Trigger of Recurrent C3 Glomerulonephritis in a Kidney Transplant Recipient

Session Information

Category: Transplantation

  • 2102 Transplantation: Clinical


  • Anwar, Amber, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Abu Kar, Sarah, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Binari, Laura, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Wang, Yihan, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Shawar, Saed, Vanderbilt University Medical Center, Nashville, Tennessee, United States

C3 Glomerulonephritis (C3GN) is a rare kidney disease caused by dysregulation of the alternative complement pathway through genetic or acquired alteration in regulatory protein. 67- 84% of kidney transplant recipients have recurrence within median time of 14-28 months and graft loss at 18 months after diagnosis. Therapy for recurrent C3GN can include immunosuppression, plasmapheresis, and complement targeting agents like Eculizumab. We present a case of recurrent C3GN in a kidney transplant recipient.

Case Description

A 57-year-old male with end-stage kidney disease secondary to C3GN on monthly Eculizumab underwent a living unrelated kidney transplant with Alemtuzumab and Solumedrol for induction. He had immediate graft function with nadir creatinine (Cr) of 1.05 mg/dL and urine protein of 0.1g/g, and maintenance immunosuppression was Tacrolimus, Mycophenolate Mofetil (MMF) and Prednisone. Two months post-transplant, he was admitted with periodontitis treated with Augmentin. Also had neutropenia which improved with 3 doses of filgrastim and transient discontinuation of MMF, Bactrim and Valcyte. He was maintained on Tacrolimus and Prednisone 10mg. At 1 week follow up, Cr was 1.9 mg/dl attributed to CNI toxicity and Tacrolimus dose was adjusted. However, he soon after developed hypertension, hematuria, proteinuria (0.75g/g), thrombocytopenia and AKI with Cr 2.7 mg/dl. An allograft biopsy was performed, showed C3GN recurrence with mesangial proliferative GN with C3-dominant and monotypic IgG4 dominant deposits. Functional complement panel showed high C3 nephritic factor (34unit/ml). He was treated with 7 plasmapheresis sessions and reinduction with Eculizumab 900mg IV weekly for 4 weeks and then 1200mg every 2 weeks. A repeat C3 nephritic factor level was undetectable. At 3 months, the Cr stabilized at 2mg/dl and proteinuria resolved.


We speculate that C3GN recurrence was triggered by infection and reduction in immunosuppression. Prompt control of disease activity can be achieved with removal of offending proteins via plasmapheresis and stabilization of complement activity with Eculizumab. Close surveillance is deemed necessary for control of disease progression.