Abstract: SA-PO0752
Minimal Change Disease and Monoclonal B-Cell Lymphocytosis: Is There an Association?
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Conlon, Luke, University of Utah Health, Salt Lake City, Utah, United States
- Abraham, Josephine, University of Utah Health, Salt Lake City, Utah, United States
- Gilligan, Sarah, University of Utah Health, Salt Lake City, Utah, United States
- Al-Rabadi, Laith, University of Utah Health, Salt Lake City, Utah, United States
- Kakani, Siddhartha, University of Utah Health, Salt Lake City, Utah, United States
Introduction
Minimal change disease (MCD) is a common cause of nephrotic syndrome that has been associated with hematologic malignancies and lymphoproliferative disorders, particularly Hodgkin lymphoma and chronic lymphocytic leukemia (CLL). Its association with monoclonal B-cell lymphocytosis is rare. We present a case of steroid-resistant MCD occurring in a patient with monoclonal B cell lymphocytosis.
Case Description
A 79-year-old woman was referred for evaluation of proteinuria and hematuria, with resolution of hematuria by the time of consultation and persistent proteinuria (UPCR 2368 mg/g). Lab studies showed hypoalbuminemia (albumin 3.2 g/dL) and preserved kidney function. Serologies & viral studies were negative. SPEP/IFE demonstrated an IgG kappa band and prior hematologic evaluation had demonstrated lymphocytosis and a peripheral blood flow cytometry was consistent with monoclonal B-cell lymphocytosis which did not meet criteria for CLL.
Kidney biopsy was consistent with MCD. Despite treatment with steroids, proteinuria persisted. Given association of MCD and lymphoproliferative disorders, evaluation for occult malignancy was pursued with PET/CT which was normal and bone marrow biopsy showed lymphoid aggregates representing 10% of marrow space and monoclonal B cells with CLL/SLL immunophenotype by flow cytometry most consistent with monoclonal B cell lymphocytosis. In light of steroid-resistant disease and the potential role of B-cell dysregulation, the patient was treated with rituximab alongside a prednisone taper. Despite disappearance of the monoclonal B cell population after receiving two doses of rituximab, the patient had persistent nephrotic range proteinuria.
Discussion
MCD occurs in up to 10% of patients with CLL, however reports associated with monoclonal B-Cell lymphocytosis are rare with only one prior case being found in the literature. In that report, rituximab and chlorambucil resulted in remission of both the B cell clone and
MCD, supporting a pathogenic relationship. In contrast, our patient's discordant renal and hematologic response raises uncertainy regarding whether the monoclonal B cell population was directly causal or merely coincidental in the development of minimal change disease. Notably, MCD is not yet a part of the spectrum of MGRS. A more consistent association between MCD and monoclonal disorders is needed to consider this a MGRS entity.