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Abstract: TH-PO157

Bevacizumab-Associated IgA-Dominant Membranoproliferative Glomerulonephritis

Session Information

Category: Trainee Case Report

  • 1500 Onco-Nephrology


  • Abu Salman, Liann, Lankenau Medical Center, Wynnewood, Pennsylvania, United States
  • Kallis, Christos, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Palmer, Matthew, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Bahrainwala, Jehan Z., University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Geara, Abdallah Sassine, University of Pennsylvania, Philadelphia, Pennsylvania, United States

Bevacizumab, a recombinant monoclonal antibody that blocks the vascular endothelial growth factor A (VEGF-A), is known to induce a renal-limited thrombotic microangiopathy (TMA), hypertension and proteinuria. A chronic bevacizumab-associated TMA can eventually lead to a glomerulopathy with membranoproliferative glomerulonephritis (MPGN) histology. We describe the unique case of IgA-dominant MPGN induced by bevacizumab in the absence of TMA.

Case Description

A 29-year-old male patient, with a history of neurofibromatosis type II and bilateral vestibular schwannomas treated with bevacizumab, is evaluated for nephrotic range proteinuria with preserved renal function eighteen months after initiation of therapy. Bevacizumab was initially held and the serologic evaluation for proteinuria was negative. The proteinuria was persistent and worsening (24h-urine protein: 6460 mg/24h) despite cessation of bevacizumab for 9 months and treatment with ACE Inhibitor eventually leading to a kidney biopsy.

The kidney biopsy showed segmental endocapillary hypercellularity with thickening of the glomerular capillary walls and segmental double contours. The immunofluorescence was positive for IgG, IgM, IgA, Kappa and Lambda with IgA dominant pattern. The electron microscopy showed subendothelial and mesangial deposits. No TMA was seen. The final diagnosis was MPGN with IgA-dominant immune complex deposition. The patient was treated with Mycophenolate Mofetil with poor response after 4 months of therapy.


VEGF-A secretion by the podocytes is essential in maintaining a healthy glomerular capillary endothelium. Disruption of this interaction by bevacizumab leads to a renal-limited TMA that is reversible after stopping the medication. Few previous case reports described IgA deposits in patients with bevacizumab-induced TMA. Previous reports of bevacizumab-associated TMA are well described, and a link between these two differing lesions may be possible but presently remain speculative. As the use of these agents is becoming more prevalent, further studies are needed to identify the mechanism and potential risk factors for renal disease to help guide treatment.