title: Patterns of noncryoglobulinemic glomerulonephritis with monoclonal Ig deposits: correlation with IgG subclass and response to rituximab.
abstract: OBJECTIVE
  Several different entities have recently been described among glomerular diseases associated with monoclonal IgG deposits. The aim of this study was to describe the distribution of the different pathologic subtypes of IgG-associated glomerulopathy and to evaluate the IgG isotype involved in these diseases.
  
  
  METHODS
  This was a retrospective study including all patients with glomerular deposits of monoclonal IgG referred to three nephrology departments between 1980 and 2008.
  
  
  RESULTS
  Twenty-six patients were included. Nephrotic syndrome was almost constantly associated with a renal dysfunction in 14 of 26 patients. The presence of M-spike was detected in only 30% of the patients, and an overt hematologic malignancy (myeloma, lymphoma) was identified in 9 of 26 patients. Patients were almost equally divided into two distinct histologic patterns: membranous nephropathy (MN) or membranoproliferative glomerulonephritis (MPGN). IgG3 deposits were identified in 80% of patients with MPGN, whereas IgG1 deposits were present in 64% of patients with MN. Ultrastructural study showed that immune deposits were nonorganized in most patients. Seven patients were treated with rituximab with excellent results: five of seven had a complete remission of the nephrotic syndrome and two of seven had a partial response. After a mean 24-month follow-up, only one patient experienced relapse of the nephropathy.
  
  
  CONCLUSIONS
  GN with monoclonal Ig deposits can be associated with MPGN or MN, which are correlated with IgG3 and IgG1 isotypes, respectively. Rituximab appears to have a very favorable benefit-to-risk ratio for patients with no overt hematologic malignancy.
authors.affiliation: Department Nephrology, Hôpital Européen Georges Pompidou, Paris, France.
authors.forename: Elsa
authors.initials: E
authors.lastname: Guiard
authors.forename: Alexandre
authors.initials: A
authors.lastname: Karras
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Plaisier
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Duong Van Huyen
authors.forename: Fadi
authors.initials: F
authors.lastname: Fakhouri
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Rougier
authors.forename: Laure-Hélène
authors.initials: LH
authors.lastname: Noel
authors.forename: Patrice
authors.initials: P
authors.lastname: Callard
authors.forename: Michel
authors.initials: M
authors.lastname: Delahousse
authors.forename: Pierre
authors.initials: P
authors.lastname: Ronco
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000032:analysis*; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use*; D001706:Biopsy; D005260:Female; D005602:France; D015432:Glomerulonephritis, Membranoproliferative / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D015433:Glomerulonephritis, Membranous / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis*; D007155:Immunologic Factors / Q000627:therapeutic use*; D007668:Kidney / Q000187:drug effects* / Q000276:immunology / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D008856:Microscopy, Fluorescence; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000188:drug therapy / Q000276:immunology; D012008:Recurrence; D012074:Remission Induction; D012189:Retrospective Studies; D000069283:Rituximab; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D007074:Immunoglobulin G; D007155:Immunologic Factors; D000069283:Rituximab