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Abstract: FR-PO1165

Recipient APOL1 High-Risk Status and the Development of FSGS in the Kidney Allograft

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Varughese, Ashok Abraham, Allegheny Health Network, Pittsburgh, Pennsylvania, United States
  • Sureshkumar, Kalathil K., Allegheny Health Network, Pittsburgh, Pennsylvania, United States

Group or Team Name

  • Allegheny Health Network Division of Nephrology
Introduction

Presence of donor homozygous APOL1 risk variant leads to inferior graft outcomes following kidney transplantation. It is thought that APOL1 high risk variants expressed in the podocytes cause injury through enhanced lysosomal membrane permeability or mitochondiral dysfunction. The impact of recipient APOL1 status on kidney allograft outcome is emerging. We present a patient with homozygous APOLI risk variant who developed collapsing FSGS in the 2nd kidney transplant from a white donor.

Case Description

A 33-year-old black male with homozygous APOL1 (G1/G1) gene expression received second kidney transplantation from a 39-year-old brain dead white female donor with 2 HLA mismatches. The 1st kidney transplant failed from thrombotic microangiopathy (TMA) thought to be triggered by severe hypertension. His biologic brother with same APOL1 mutation developed kidney failure from TMA and is awaiting kidney transplantation. For the second transplant, patient received induction with Thymoglobulin followed by tacrolimus/MMF/prednisone maintenance & standard infection prophylaxis. Serum creatinine reached a baseline of 0.9-1.0 mg/dL. Two years post-transplant, the patient started experiencing worsening proteinuria to nephrotic range. Allograft biopsy revealed collaping FSGS (figure 1). Secondary work was negative for paraproteinemia and infections including CMV, BK, parvovirus, HIV, hepatitis B & C . He was started on olmesartan and empagliflozin. Serum creatinine remains at 1.1 mg/dl.

Discussion

Donor APOL1 high risk status adversely impact kidney transplant outcomes. Our case points to an association between recipent APOL1 high risk variant and the development of collapsing FSGS in the renal allograft. A "second hit" could be a trigger. An association between recipient APOL1 status and inferior kidney allograft outcome from heightened alloimmune respone was reported previously.

Acknowledgment

Authors declare no relevant financial disclosures