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Abstract: TH-PO0772

A Tale of Two Patterns of Membranoproliferative Glomerulonephritis Associated with Chronic Lymphocytic Leukemia

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Adisa, Oluwadamilola, Johns Hopkins University, Baltimore, Maryland, United States
  • Singh, Aditi, Johns Hopkins University, Baltimore, Maryland, United States
  • Acharya, Veena K., Johns Hopkins University, Baltimore, Maryland, United States
  • Cervantes, C. Elena, Johns Hopkins University, Baltimore, Maryland, United States
  • Rosenberg, Avi Z., Johns Hopkins University, Baltimore, Maryland, United States
  • Bagnasco, S.M., Johns Hopkins University, Baltimore, Maryland, United States
  • Hanouneh, Mohamad A., Johns Hopkins University, Baltimore, Maryland, United States
Introduction

Renal involvement in chronic lymphocytic leukemia (CLL) may present as glomerulonephritis (GN), interstitial nephritis, or direct infiltration. GN commonly appears as MPGN or minimal change disease, potentially causing nephrotic syndrome and renal insufficiency.

Case Description

A 75-year-old male presented with acute kidney injury (AKI) with serum creatinine (Scr) 1.4 mg/dl, urine protein-to-creatinine ratio (UPCR) 1,136 mg/g, and microscopic hematuria. Renal biopsy revealed MPGN with monoclonal immunoglobulin (Ig) deposits of IgG3 kappa type (Fig 1). Bone marrow biopsy confirmed a diagnosis of variant CLL characterized by a monoclonal kappa-restricted CD5-positive B-cell population. He was treated with Acalabrutinib, with remission and normalizing of Scr and UPCR.

Two years later, he presented with nephrotic syndrome (UPCR 14,327 mg/g), microscopic hematuria, and AKI (Scr 1.96 mg/dL). Renal biopsy showed MPGN with polyclonal Ig deposits and focal interstitial infiltrates of CD20 and CD5-positive mononuclear cells (Fig 2). Bendamustine and Rituximab induction improved AKI and reduced UPCR to 2,281 mg/g.

Discussion

MPGN associated with CLL is commonly linked to monoclonal Ig deposition (like first presentation), with rare cases exhibiting a polyclonal pattern as seen in the second presentation. The pathogenesis involves several mechanisms: direct infiltration of the kidneys by leukemic cells, deposition of monoclonal Ig within the glomeruli, and/or immune complex deposition. These processes trigger immune-mediated injury to the glomeruli. Treatment is directed at the underlying hematologic malignancy, often resulting in disease remission in the kidneys.

Digital Object Identifier (DOI)