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Abstract: SA-PO1132

De Novo Cytomegalovirus-Triggered FSGS After Kidney Transplantation Associated with APOL1 Risk Allele

Session Information

Category: Trainee Case Report

  • 1902 Transplantation: Clinical


  • Gupta, Mallika, Washington University in St. Louis, Saint Louis, Missouri, United States
  • Java, Anuja, Washington University in St. Louis, Saint Louis, Missouri, United States

Recurrent and de novo glomerulonephritis (GN) account for 18% to 22% of death-censored kidney allograft failures. We report a case of de novo cytomegalovirus (CMV)-associated FSGS after kidney transplantation from an African American (AA) donor.

Case Description

A 52-yr-old White female (WF) with ESRD secondary to HTN underwent a 4-antigen mismatched, CMV D+/R-, deceased donor renal transplant from a 43-yr-old AA male in July 2018. Induction immunosuppression included methylprednisolone and Thymoglobulin followed by tacrolimus, mycophenolic acid (MMF) and prednisone. Serum creatinine (Cr) was 1 mg/dl at discharge. In Feb 2019, the patient presented with abdominal pain, diarrhea, and fever. Creatinine was 1.3 mg/dl, which worsened to 7.9 mg/dl over 5 days. Spot urine protein creatinine ratio (UPC) was 15. Infectious workup revealed CMV viremia (29,7460 IU/ml). Patient had discontinued valganciclovir (VGCV) 3 months after transplant. Allograft biopsy revealed podocyte effacement. Despite treatment for the CMV viremia (VGCV 900 mg po qd and discontinuation of MMF), Cr worsened and hemodialysis (HD) was initiated. VGCV was switched to IV ganciclovir 3 x wk with HD leading to clearance of viremia. Creatinine improved and HD was discontinued in April 2019. UPC improved to 7. Biopsy tissue sent for APOL1 risk variant genotyping revealed compound heterozygosity for G1/G2.


Approximately 13% of AA carry two APOL1 risk variants. Increased risk of graft loss following kidney transplantation is associated with these alleles. However a second hit is required. Mechanisms for CMV-induced podocytopathy via injury to permeability barrier have been postulated. Our case exemplifies CMV as a second hit causing podocytopathy in a recipient with heterozygosity for APOL1 in an AA donor. Studies to better understand the mechanisms and predisposing factors for APOL1-associated kidney diseases are critical since recipients from donors with the risk alleles may warrant tailored management. Of note, the mate kidney was transplanted in a 48-yr-old WF who recently completed the 9-month CMV prophylaxis. Questions arise: 1) Should the duration of viral prophylaxis be extended in the second patient, 2) Should increased frequency of viremia screening be considered and, 3) Should aggressive antiviral strategies be considered at first identification of viremia?