Kidney Week

Abstract: SA-PO0696

Immunotactoid Glomerulopathy in a Patient with Diffuse Large B-Cell Lymphoma and Untreated Hepatitis C

Session Information

• Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
  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

• Helderlein, Philip John, Medical University of South Carolina, Charleston, South Carolina, United States

Philip John Helderlein, DO

• Gerardot, Shori, Medical University of South Carolina, Charleston, South Carolina, United States

Shori Gerardot, MD

• Budisavljevic, Milos N., Medical University of South Carolina, Charleston, South Carolina, United States

Milos N. Budisavljevic, MD, FASN

• Fulop, Tibor, Medical University of South Carolina, Charleston, South Carolina, United States

Tibor Fulop, MD, PhD, FASN

Introduction

Immunotactoid glomerulopathy (ITG) is a rare condition characterized by the deposition of microtubules into the glomerulus resulting in a membranoproliferative glomerulonephritis (MPGN). We present a case of ITG-related MPGN resulting in dialysis dependence in a patient with diffuse large B-cell lymphoma (DLBCL) and untreated hepatitis-C (HCV). The case provides an insight into the diagnostic challenges when two potential etiologies coexist.

Case Description

A 66-year-old male with DLBCL and untreated HCV presented with 5-7 days of anuria and serum creatinine >7 mg/dL (baseline 1.3 mg/dL) requiring dialysis in the setting of hyperkalemia and clinical uremia. Renal biopsy revealed a diffuse, crescentic MPGN with prominent exudative features and fibrinoid necrosis. Immunofluorescence revealed strong IgG and k light chain restriction with weak/trace IgA, IgM, and l signals. EM showed 37-45 nm, hollow core, organized microtubular deposits. Congo red staining was negative for amyloid and C68 highlighted increased intracapillary macrophages. Additional serologic studies returned with negative rheumatoid factor and cryoglobulins; normal C4 (15.9 mg/dL) but low C3 (38.2 mg/dL) and IgG k monoclonal protein measuring 0.65 g/dL on protein electrophoresis. HCV viral load 295,842 measured copies/mL.

Discussion

The case demonstrates the diagnostic complexity when attempting to distinguish between monoclonal ITG and cryoglobulinemic GN. The serologic studies in the case presented favor ITG as opposed to type I cryoglobulinemic GN in the presence of a monoclonal spike on protein electrophoresis, low C3, normal C4, and negative cryoglobulins. The pathologist noted these two processes may exist in a spectrum. The diagnosis was based on electron microscopy measurements of tubular deposits in the glomerulus described as organized, 37-45 nm, hollow core structures. Given the co-existence of DLBCL and untreated HCV, a unifying physiological cascade is hypothesized: with HCV leading to clonal B-cell proliferation and DLBCL. Subsequently, DLBCL led to a monoclonal IgG k production, which produced organized microtubule deposits in the glomerulus presenting as crescentic MPGN.

Ultimately, this case presents the unifying diagnosis of two, seemingly different processes as one single nephrology diagnosis; with untreated HCV leading to DLBCL and ITG, manifesting as MPGN on renal biopsy.