ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO2212

Is One Allele Enough to Cause APOL1-Associated Nephropathy?

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical


  • Johnson, Peace, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Bobba, Sindhura, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Paluri, Sravanthi, Virginia Commonwealth University Health System, Richmond, Virginia, United States
  • Gupta, Gaurav, Virginia Commonwealth University Health System, Richmond, Virginia, United States

The high risk APOL1 genotype are associated with an increased risk of developing non-diabetic kidney disease. In the post-kidney transplant setting, a high-risk donor APOL1 genotype (but not recipient genotype) is associated with an increased risk of graft failure and proteinuria, indicating that it is local glomerular APOL1 gene expression that confers disease rather than systemic gene expression. Here, we present 2 patients that developed post-transplant focal segmental glomerulosclerosis (FSGS) after an initial diagnosis and treatment of Antibody-mediated rejection (AMR).

Case Description

Two patients with end stage kidney disease, highly sensitized, received deceased donor kidney transplants from African American donors (one in 2019 and the other a regraft in 2020). Donors were without discernable proteinuria on urine dipstick. Initial post tranasplant courses were complicated by AMR treated as per center protocol. Tissue-based whole biopsy gene expression studies on kidney biopsy specimens (MMdx, using Molecular Microscope, Alberta, Canada) confirmed AMR along with grossly elevated interferon-γ gene expression. Subsequently each developed nephrotic range proteinuria with biopsy-confirmed FSGS and ongoing AMR .

In both patients, in the absence of a prior history of FSGS and a delayed development of proteinuria in the first case (2019, patient1), an absence of recurrence in the first allograft in the second case (2020, patient2), a diagnosis of donor-derived APOL-1 nephropathy was considered and retrospective donor genotyping revealed the intermediate G1/G0 genotype. See Figure for more details.


We hypothesize that extreme local interferon-γ activation due to AMR was the primary trigger that could have resulted in local APOL-1 gene activation and subsequent podocytopathy. Similar data was recently reported by Shetty et al, in a kidney transplant patient with COVID associated collapsing nephropathy and G1/G0 donor genotype. Based upon these data we hypothesize that the G1/G0 genotype may represent intermediate risk for podocytopathies. Further research is needed in this area to confirm these initial associations.