title: Effect of single-dose rituximab on primary glomerular diseases.
abstract: BACKGROUND
  A paradigm shift from such toxic 'nonspecific' therapies to selective immunomodulating regimens is necessary for glomerular diseases. Rituximab, which acts by inhibiting CD20-mediated B cell proliferation and differentiation, could be effective in the treatment of nephrotic syndrome as shown in recent reports.
  
  
  METHODS
  To assess the effects of rituximab in patients with primary glomerular diseases, including minimal-change disease, immunoglobulin A (IgA) nephropathy, focal segmental glomerulonephritis, membranous nephropathy and membranoproliferative glomerulonephritis, we performed a prospective trial of the effects of single-dose rituximab therapy in 24 patients. We prospectively evaluated the serum and urinary biochemical parameters before and after 6 months of therapy.
  
  
  RESULTS
  In all of the patients studied, depletion of CD19 and CD20 cells was noted, with significant reduction in the degree of proteinuria from 3.7 ± 3.4 g/day at baseline to 1.3 ± 2.0 g/day at 6 months after the drug administration (p = 0.002). However, no significant changes of the serum creatinine, urinary RBC sediment, serum CD4/8 or serum IL-4 levels were observed at 6 months after the drug administration. In subjects with IgA nephropathy, while depletion of CD19 and CD20 cells was noted, no significant change in the severity of proteinuria was observed at 6 months after the drug administration as compared with the level at the baseline.
  
  
  CONCLUSIONS
  For the treatment of primary glomerular diseases, the use of a single dose of rituximab is demonstrated with no serious adverse events. Further study of the mechanism of action of rituximab in successfully treated patients could encourage new perspectives in the treatment of primary glomerular diseases.
authors.affiliation: Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Sugiura
authors.forename: Takashi
authors.initials: T
authors.lastname: Takei
authors.forename: Mitsuyo
authors.initials: M
authors.lastname: Itabashi
authors.forename: Misao
authors.initials: M
authors.lastname: Tsukada
authors.forename: Takahito
authors.initials: T
authors.lastname: Moriyama
authors.forename: Chiari
authors.initials: C
authors.lastname: Kojima
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Shiohira
authors.forename: Ari
authors.initials: A
authors.lastname: Shimizu
authors.forename: Yuki
authors.initials: Y
authors.lastname: Tsuruta
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Amemiya
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Ogawa
authors.forename: Keiko
authors.initials: K
authors.lastname: Uchida
authors.forename: Ken
authors.initials: K
authors.lastname: Tsuchiya
authors.forename: Kosaku
authors.initials: K
authors.lastname: Nitta
mesh_terms: D000328:Adult; D058846:Antibodies, Monoclonal, Murine-Derived / Q000008:administration & dosage* / Q000009:adverse effects; D004305:Dose-Response Relationship, Drug; D005260:Female; D005921:Glomerulonephritis / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D006801:Humans; D007155:Immunologic Factors / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D000069283:Rituximab; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D007155:Immunologic Factors; D000069283:Rituximab