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Abstract: PO1890

Proliferative Glomerulonephritis with Monoclonal Immunoglobulin Deposits: Searching for the Underlying Clone

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Javaugue, Vincent, Centre Hospitalier Universitaire de Poitiers, Poitiers, France
  • Pascal, Virginie, Centre Hospitalier Universitaire de Limoges, Limoges, France
  • Bender, Sébastien, Centre National de la Recherche Scientifique, Limoges, France
  • Goujon, Jean-Michel, Centre Hospitalier Universitaire de Poitiers, Poitiers, France
  • Touchard, Guy, Centre Hospitalier Universitaire de Poitiers, Poitiers, France
  • Sirac, Christophe, Centre National de la Recherche Scientifique, Limoges, France
  • Bridoux, Frank, Centre Hospitalier Universitaire de Poitiers, Poitiers, France

Group or Team Name

  • Centre national de référence amylose AL et autres maladies par dépôts d'Ig monoclonales

The pathophysiological mechanisms of proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) are still largely unknown. Only 30% of PGNMID cases have a detectable circulating monoclonal immunoglobulin (Ig) and a bone marrow corresponding clone.


We reviewed a French cohort of PGNMID with particular focus on hematological characteristics. A high-throughput sequencing assay from bone marrow and/or blood mRNA encoding immunoglobulins (RACE-RepSeq) was used to detect the underlying clone.


Seventy-one patients (M/F ratio=1.6, median age 59 years) were included. At diagnosis, 73% had renal insufficiency (median serum creatinine=1.7 mg/dL). All patients had proteinuria, with nephrotic syndrome in 59% and microscopic hematuria in 85% of cases. No patient had extra-renal manifestations. By light microscopy, kidney biopsy revealed membranoproliferative glomerulonephritis (74%), mesangial glomerulonephritis (14%) or membranous glomerulonephritis (12%). By immunofluorescence (IF), deposits stained for IgG in 55 cases (mostly IgG3κ), IgM in 7 cases, IgA in 4 cases or light chain (LC) only in 5 cases. Serum and/or urine immunofixation was positive in 26 cases (37%). An underlying clone was found in 21 cases (30%) using bone marrow or blood flow cytometry analysis. The clonal detection rate was particularly low in IgG3κ-PGNMID (9%). The nature of the clone differed with PGNMID subtype: lymphoplasmacytic in IgM-PGNMID, and plasmacytic in IgA/LC-PGNMID. RACE-RepSeq analysis failed to detect a bone marrow or blood clone in 18/26 cases (IgG3κ-PGNMID, n=17; IgGAκ-PGNMID, n=1). IF analysis of kidney samples using anti-Vκ antibodies showed positive staining for Vκ1, Vκ2, Vκ3 and Vκ4 in 3/3 tested IgG3k-PGNMID patients without a detectable clone, whereas deposits stained only for Vκ2 in one IgG1k-PGNMID patient who had a bone marrow Vκ2 clone by RACE-RepSeq analysis.


These results suggest that PGNMID is a heterogeneous medical condition and that some cases might involve oligoclonal production of nephrotoxic Ig restricted to the IgG3k isotype. Such cases should no longer be classified as MGRS.