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Abstract: TH-PO0444

Proliferative Glomerulonephritis with Monoclonal IgG Kappa Deposits in Acute HIV Infection Without Detectable Clonal Disorder

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

  • Alqudah, Zain Mohamad, SUNY Upstate Medical University, Syracuse, New York, United States
  • Rehman, Tanzeel, SUNY Upstate Medical University, Syracuse, New York, United States
  • Irfan, Babar, SUNY Upstate Medical University, Syracuse, New York, United States
  • Hashemi, Sara, SUNY Upstate Medical University, Syracuse, New York, United States
  • Nawaz, Iqra, SUNY Upstate Medical University, Syracuse, New York, United States
  • Habib, Muhammad Farhan, SUNY Upstate Medical University, Syracuse, New York, United States
Introduction

PGNMID is a rare entity within MGRS, characterized by monoclonal Ig deposition in the kidney. Most cases lack detectable circulating monoclonal proteins or identifiable clonal disorders, complicating diagnosis and management. HIV, acts as a potential triggers.

Case Description

29-year-old man with T1DM presented with hypoxemic respiratory failure & new nonischemic cardiomyopathy (LVEF 35%). Course was complicated by transfusion-dependent normocytic anemia with MAHA. UA showed hematuria and nephrotic-range proteinuria; kidneys were enlarged. Serologic workup was negative except for newly diagnosed HIV (viral load 522,495 copies/mL, CD4 <9%). TMA evaluation (normal ADAMTS13, platelets, complement, negative genetic testing) and negative Coombs, PNH, and extensive hematologic studies excluded TTP, HUS, DIC, and malignancy.Kidney biopsy demonstrated diffuse proliferative glomerulonephritis with monotypic IgG kappa deposits (PGNMID). IF showed IgG-kappa restriction with C3; EM revealed mesangial, subendothelial, and focal subepithelial deposits, GBM thickening, podocyte effacement, and tubuloreticular inclusions.

Discussion

This case highlights PGNMID as a renal-limited manifestation of MGRS without detectable clonal disease. Despite extensive hematologic evaluation (bone marrow, lymph node biopsy, cytogenetics, FISH, mutation panels), no clone was identified, consistent with reported detection rates (~30%). Concurrent HIV infection adds diagnostic complexity, given its association with diverse renal pathologies (HIVAN, immune complex disease, TMA) and polyclonal B-cell activation. Biopsy confirmed PGNMID with monotypic IgG kappa deposits in a proliferative pattern. with Tubuloreticular inclusions, suggesting infection-triggered clonal or oligoclonal B-cell activation. Concern for TMA ruled out with normal ADAMTS13, plts, and complement levels, along with negative biopsy findings, argue against primary TMA.

Monotypic Kappa chain deposition on IF.