title: Decrease in serum antiphospholipid antibody levels upon development of nephrotic syndrome in patients with systemic lupus erythematosus: relationship to urinary loss of IgG and other factors.
abstract: OBJECTIVE
  Having observed a decrease in antiphospholipid antibodies (aPL) upon the development of nephrotic syndrome, as well as a negative association between nephrotic syndrome and secondary antiphospholipid syndrome, in patients with systemic lupus erythematosus (SLE), we sought to determine if this could be due to urinary loss of aPL and/or other factors.
  
  
  METHODS
  IgG and IgM aPL as well as other autoantibodies were studied by enzyme-linked immunosorbent assay with cardiolipin as antigen in serum and urine from six patients with SLE who had elevated serum aPL levels and developed nephrotic syndrome (cases). For controls, we studied: (1) three SLE patients with nephrotic syndrome but low aPL levels; (2) three patients with non-SLE nephrotic syndrome; (3) three SLE patients with high-titer aPL but no proteinuria; and (4) 10 healthy volunteers.
  
  
  RESULTS
  We found urinary IgG, but no IgM, aPL in all cases and in one control from Group 2. Serum IgG aPL had gradually decreased after the development of nephrotic syndrome and had become normal. IgM aPL had also decreased in the four patients who had elevated levels, having reached normal levels at the time of the study in two. There was an apparent correlation between serum and urine IgG aPL levels but not between urinary IgG aPL and total proteinuria. By Farr's method, we found no urinary anti-DNA despite high serum titers in three cases. The two cases and one of the controls in Group 1 who had serum antibodies to extractable antigens also had these antibodies in the urine.
  
  
  CONCLUSIONS
  Urinary loss of IgG aPL during nephrotic syndrome does not completely explain the reduction in serum aPL, since IgM also decreases. There could also be decreased synthesis and/or increased catabolism of immunoglobulins.
authors.affiliation: Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico.
authors.forename: M E
authors.initials: ME
authors.lastname: Pérez-Vázquez
authors.forename: J
authors.initials: J
authors.lastname: Cabiedes
authors.forename: A R
authors.initials: AR
authors.lastname: Cabral
authors.forename: D
authors.initials: D
authors.lastname: Alarcón-Segovia
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000032:analysis*; D001769:Blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis / Q000652:urine*; D007132:Immunoglobulin Isotypes / Q000032:analysis / Q000652:urine; D007075:Immunoglobulin M / Q000032:analysis / Q000652:urine; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000652:urine; D009404:Nephrotic Syndrome / Q000276:immunology* / Q000473:pathology / Q000652:urine; D010743:Phospholipids / Q000276:immunology*; D011507:Proteinuria / Q000276:immunology / Q000652:urine
chemical_list: D001323:Autoantibodies; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes; D007075:Immunoglobulin M; D010743:Phospholipids