title: Proteinuria in rats induced by serum from patients with collapsing glomerulopathy.
abstract: BACKGROUND
  Primary collapsing glomerulopathy recurs postransplant, raising the possibility of circulating factors implicated in the pathogenesis of the disease.
  
  
  METHODS
  To determine the presence of circulating factors in collapsing glomerulopathy patients, we tested serum from those patients in an in vivo assay. Eleven groups of rats received serum from collapsing glomerulopathy patients, idiopathic focal segmental glomerulosclerosis (FSGS) or healthy subjects in its native form, isolated IgG, or serum without IgG. The presence of proteinuria and creatinine clearance were determined. Histopathologic analysis included light, immunofluorescence, and electron microscopy.
  
  
  RESULTS
  Collapsing glomerulopathy rats developed proteinuria while rats injected with serum from FSGS and healthy subjects did not. Rats injected with serum of collapsing glomerulopathy in its native form developed marked proteinuria (99.2 +/- 42 mg/24 hours at day 5, P= 0.0001, compared to the baseline), and decreased in creatinine clearance. Rats receiving isolated IgG or serum without IgG from collapsing glomerulopathy developed mild proteinuria (46.5 +/- 8.4 mg/24 hours and 30.9 +/- 11 mg/24 hours, respectively, at day 5 (P= 0.0001). Glomerular tuft retraction and podocyte damage were seen only in collapsing glomerulapthy rats. No abnormalities were found in rats injected with serum from FSGS or healthy subjects.
  
  
  CONCLUSIONS
  Circulating factors in the serum of collapsing glomerulopathy patients produce podocyte damage, whereas such factors are not present in noncollapsing FSGS. IgG eluates from collapsing glomerulopathy produce proteinuria when injected into the rat. Such factors remain in the circulation when serum of patients is adsorbed into protein A, raising the possibility that there are more than one circulating factor present in patients with collapsing glomerulopathy.
authors.affiliation: Department of Pathology, Instituto Nacional de Cardiologia Ignacio Chavez, Mexico City, Mexico. mcavila@cardiologia.org.mx
authors.forename: Maria del Carmen
authors.initials: Mdel C
authors.lastname: Avila-Casado
authors.forename: Israel
authors.initials: I
authors.lastname: Perez-Torres
authors.forename: Ari
authors.initials: A
authors.lastname: Auron
authors.forename: Virgilia
authors.initials: V
authors.lastname: Soto
authors.forename: Teresa I
authors.initials: TI
authors.lastname: Fortoul
authors.forename: Jaime
authors.initials: J
authors.lastname: Herrera-Acosta
mesh_terms: D000293:Adolescent; D000327:Adsorption; D000328:Adult; D000368:Aged; D000818:Animals; D003404:Creatinine / Q000097:blood / Q000652:urine; D004591:Electrophoresis, Polyacrylamide Gel; D005923:Glomerulosclerosis, Focal Segmental / Q000097:blood; D006801:Humans; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000097:blood; D007267:Injections; D007668:Kidney / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000097:blood* / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology / Q000648:ultrastructure; D008854:Microscopy, Electron; D008875:Middle Aged; D011507:Proteinuria / Q000209:etiology*; D051381:Rats; D013205:Staphylococcal Protein A
chemical_list: D007074:Immunoglobulin G; D013205:Staphylococcal Protein A; D003404:Creatinine