Abstract: FR-PO0473
Native Kidney BK Nephropathy from Intravenous Immunoglobulin (IVIG) Infusions: A Rare Clinical Entity
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Tsai, Joseph M., Southwest Healthcare Medical Education Consortium, Temecula, California, United States
- Pidugu, Varsha, Southwest Healthcare Medical Education Consortium, Temecula, California, United States
- Chang, David, Southwest Healthcare Medical Education Consortium, Temecula, California, United States
- Quach, Duc Hong, Southwest Healthcare Medical Education Consortium, Temecula, California, United States
Introduction
BK nephropathy is one of the most common complications for renal transplant patients. Treatment usually starts with stepwise reduction of immunosuppression therapy, with IVIG infusions as a possible adjunct therapy. It’s notable, however, that BK nephropathy can also afflict patients with native kidneys. Here we present a case of BK nephropathy from IVIG infusions in a patient with Diffuse Large B-cell Lymphoma.
Case Description
67-year old male with history of DLBCL, status post chemotherapy and immunotherapy with CAR T-cell therapy years ago, currently on IVIG infusions for B-cell Aplasia, Hypertension and T2DM presented to the clinic after hospitalization for AKI and to follow up on renal biopsy. Previously presented to the clinic for worsening renal function and serum creatinine was 1.24 on initial presentation. Jardiance was started and then down-titrated with no preservation of renal function. Subsequent hospitalization found his serum creatinine increased to 4.21, UACR 253 mg/g and UPCR 593 mg/g with negative ANA panel. Renal biopsy revealed viropathic changes and viral particles were identified in the cortical tubules. SV40/CMV stain revealed BK nephropathy. His monthly IVIG infusions were promptly held after discussion with hematologist/oncologist. Patient’s CKD eventually progressed to stage 4 and later required hemodialysis.
Discussion
IVIG has pleiotropic effects on the immune system: with higher dosage it causes immunosuppression by saturating the Fcγ receptor binding sites, in addition to inhibiting C3b, C4b complement components, which are critical among its many immunosuppressive downstream effects. At lower doses, it tends to exert immunoenhancing effects by facilitating opsonization, resulting in complement promotion and dendritic cell activation. It is likely that the low dose IVIG administration in our patient caused a rare Fcγ receptor saturation, which in turn induced downregulation of ADCC (antibody dependent cellular cytotoxicity) function of NK cells and suppressed T-cell function via decreased antigen presentation, leading to BK virus activation. While IVIG usually confers therapeutic properties against BK virus, in a rare case, it can play a major role in the proliferation of BK virus. Heightened vigilance against opportunistic infections should be exercised on patients on immunomodulatory therapy, despite atypical presentations.