Kidney Week

Abstract: FR-PO1276

Paraneoplastic Atypical Anti-GBM Nephritis Associated with Diffuse Large B-Cell Lymphoma

Session Information

• Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Onconephrology

• 1600 Onconephrology

Authors

• Alexander, Brooke, University of Miami Miller School of Medicine, Miami, Florida, United States

Brooke Alexander, DO

• Villa, Eduardo Arturo, University of Miami Miller School of Medicine, Miami, Florida, United States

Eduardo Arturo Villa, MD

• Nasr, Samih H., Mayo Clinic Minnesota, Rochester, Minnesota, United States

Samih H. Nasr, MD

• Zuo, Yiqin, University of Miami Miller School of Medicine, Miami, Florida, United States

Yiqin Zuo, MD, PhD

• Naranjo, Christopher D., University of Miami Miller School of Medicine, Miami, Florida, United States

Christopher D. Naranjo, DO

• Alonso, Shawn, University of Miami Miller School of Medicine, Miami, Florida, United States

Shawn Alonso, DO

• Drexler, Yelena, University of Miami Miller School of Medicine, Miami, Florida, United States

Yelena Drexler, MD, MS, FASN

Introduction

Atypical anti-glomerular basement membrane (GBM) nephritis is a rare entity characterized by linear IgG deposition along the GBM without diffuse crescentic glomerulonephritis or detectable circulating anti-GBM antibodies. It has been associated with smoking but has not been reported as a paraneoplastic glomerulopathy. We describe a case of atypical anti-GBM nephritis, polytypic variant, arising in the setting of diffuse large B-cell lymphoma (DLBCL) with concurrent renal and oncologic response to lymphoma-directed therapy.

Case Description

A 76-year-old woman with a history of smoking, lupus-like syndrome, and low-grade B-cell lymphoma with plasmacytic differentiation was admitted for chemotherapy initiation following transformation to DLBCL. She presented with acute kidney injury (serum creatinine 2.0 mg/dL), nephrotic syndrome (urine protein-to-creatinine ratio 15 g/g, serum albumin 2.7 g/dL), and microscopic hematuria. Autoimmune serologic workup was negative, including anti-GBM antibodies. Serum protein electrophoresis and immunofixation detected a gamma heavy chain paraprotein (M-spike 0.1 g/dL) with a normal serum free kappa/lambda ratio (1.31). Renal function continued to decline (serum creatinine 4.1 mg/dL), prompting kidney biopsy. Biopsy demonstrated diffuse linear polytypic IgG staining of glomerular basement membranes with a membranoproliferative and mesangial sclerosing pattern without crescents, consistent with atypical anti-GBM nephritis. Following three cycles of pola-R-CHP (polatuzumab, rituximab, cyclophosphamide, doxorubicin, and prednisone), interval PET/CT demonstrated marked reduction in FDG-avid lymphadenopathy. Concurrently, serum creatinine improved to 1.43 mg/dL, with proteinuria decreasing to 9 g/g.

Discussion

Parallel improvement in renal function and lymphoma burden supports a paraneoplastic glomerulopathy, potentially related to immune cross-reactivity between tumor antigen and GBM epitopes. Polytypic IgG staining argues against monoclonal immunoglobulin deposition disease. The absence of circulating anti-GBM antibody and absence of diffuse crescentic phenotype distinguish this from classic anti-GBM nephritis and poses a challenge for monitoring treatment response. This case expands the spectrum of paraneoplastic glomerulopathies in hematologic malignancies and underscores the importance of kidney biopsy in establishing the diagnosis.