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Abstract: SA-PO869

Collapsing Focal Segmental Glomerulosclerosis Complicating BK Allograft Nephropathy in a Heart-Kidney Transplant Recipient

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Zamir, Zamir Ahmed, Chicago State University, Chicago, Illinois, United States
  • Josephson, Michelle A., The University of Chicago Medicine, Chicago, Illinois, United States
  • Kyeso, Yousuf, The University of Chicago Medicine, Chicago, Illinois, United States
  • Krishnamoorthy, Sambhavi, The University of Chicago Medicine, Chicago, Illinois, United States
  • Cunningham, Patrick, Chicago State University, Chicago, Illinois, United States
Introduction

Collapsing focal segmental glomerulosclerosis (FSGS) is a variant of FSGS and is associated with severe nephrotic syndrome and acute kidney injury and can occur after kidney transplantation. The exact mechanism of collapsing FSGS after kidney transplantation is unclear, but potential causes include autoimmune diseases, cancers, medications side effects, and viral infections. We describe a unique presentation of this detrimental diagnosis in kidney transplantation.

Case Description

47-year old South East Asian male with ESRD secondary to DM and ischemic cardiomyopathy underwent HLA compatible simultaneous heart and kidney transplant. Nadir serum Cr was 1.5 mg/dl. Induction with Basiliximab and immunosuppression included Tacrolimus, Prednisone and Mycophenolate Mofetil (MMF). Four months after transplant, serum Cr peaked at 3 mg/dl and BK plasma viral load (VL) found to be 2 million copies per ml. Kidney biopsy confirmed BK nephropathy. MMF replaced with leflunomide, and IVIG 2g/kg were given. Three months later, serum Cr stabilized at 2 mg/dl and BK VL improved to 30,000 copies. Six months later, patient presented with acute onset hypervolemia, proteinuria of 18 grams, and oliguric AKI with Cr of 5.5 mg/dl. Repeat kidney biopsy revealed collapsing FSGS on pathology with diffuse podocytes effacement on electron microscopy. BK VL increased to 900,000 copies, and infectious workup was negative. Patient required hemodialysis for hypervolemia, IVIG 2g/kg, FK goal was lowered to 3-5 ng/ml, and empiric 3 sessions of plasmapheresis were instituted for a concern of de novo FSGS. Six weeks later, patient was able to be weaned off HD, serum Cr stabilized at 3.5 mg/dl, and urine protein improved to 1 mg/dl. Repeat BK VL came down to 35000 copies/ml.

Discussion

Here, we present a case of acute nephrotic syndrome secondary to collapsing FSGS 12 months post kidney transplantation. Patient has no known history of FSGS nor any evidence of autoimmune diseases or malignancy. He had no exposure to any new medication and his infectious workup was negative except for BK viremia. We believe that collapsing FSGS was triggered by the significant BK viremia and nephropathy in this case. Early detection of proteinuria and prompt treatment of BK viremia can potentially reverse this catastrophic sequel.