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Abstract: SA-PO853

Aliskiren as an Adjunct Treatment for Recurrent C3 Glomerulonephritis (C3GN) in a Transplant Patient

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Akbar, Nouman, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Muthusamy, Selvaraj, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Kamal, Layla, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Moinuddin, Irfan Ahmed, Virginia Commonwealth University Health System, Richmond, Virginia, United States
Introduction

C3GN is an immune complex disease mediated by activation of alternative complement pathway. This pathway can be activated by renin resulting in cleavage of C3, thus producing C3 convertase and subsequent membrane attack complex formation. Aliskiren, a direct renin inhibitor, can inhibit the complement and in a recent case report was successfully used for a case of native kidney C3GN.

Case Description

25 years old African-American female with end-stage renal disease due to biopsy proven C3GN had a living unrelated kidney transplant at our center. Her pre-transplant testing showed elevated levels of complement fragments Ba/Bb and soluble C5b-9 but no pathogenic genetic mutations. C3 nephric factor and Factor H autoantibody were negative. She received induction with anti-thymocyte globulin, and maintenance immunosuppression was tacrolimus, mycophenolate mofetil (MMF) and prednisone. A surveillance biopsy at 3 months post-transplant did not show rejection or recurrence of primary disease. She developed 1.5 g/d proteinuria 3 years post-transplant while on losartan. A kidney biopsy showed recurrent C3GN, with immune complex deposits on electron microscopy. Her repeat testing was negative for C3 nephric factor and Factor H autoantibody. The complement fragments Ba/Bb and soluble C5b-9 levels were normal possibly due to her baseline immunosuppression. She was switched from losartan to Aliskiren and her MMF dose was increased by 500mg/d. Her proteinuria improved to 0.2 g/d over the next 8 months. A post-treatment biopsy was performed. Comparison of pre- and post-biopsy data showed a statistical reduction (p<0.01) in the mean (SD,standard deviation) size of deposits [2201 nanometer (SD 1102) vs 884 nm (SD 255)] as well as the density of deposits [3.8 per capillary loop (SD 2.5) vs 2.5 per capillary loop (SD 2.8)]

Discussion

Traditionally management of C3GN has included immunosuppressive agents including steroids, MMF and a possible role of complement pathway blocker, eculizumab. There have been case reports of successful treatment of native kidney C3GN in children with Aliskiren and MMF. In this first report we describe achievement of complete remission in a patient with recurrent C3GN after kidney transplant with Aliskiren and MMF intensification. These data support further trials for this relatively cheap therapy in this rare disease space.