title: Increased prevalence of anti-gliadin IgA-antibodies with aberrant duodenal histopathological findings in patients with IgA-nephropathy and related disorders.
abstract: BACKGROUND
  Antibodies present in coeliac disease may occur in IgA-nephropathy. This raises the question of food intolerance in the disease. Evidence for a true correlation between the two disorders has however been scarce.
  
  
  METHODS
  Sera from 89 patients with IgA-nephropathy and 13 other patients with IgA deposits in the glomeruli of kidney biopsies were analysed for IgA-antibodies to gliadin, endomysium and tissue transglutaminase (92/102 patients).
  
  
  RESULTS
  Eleven out of 89 (12.4%) of the patients with IgA-nephropathy and five of the 13 others (38%) had elevated titres of IgA-antibodies to gliadin but, in all cases but one, normal IgA-antibodies to endomysium. Patients with IgA-nephropathy and elevated IgA-antibodies to gliadin had elevated total serum IgA more frequently than patients who had not (p<0.01). Two patients with IgA-nephropathy and one with Hennoch Schönlein's purpura had elevated IgA-antibodies to tissue transglutaminase. Small bowel biopsy in 7 out of 11 IgA-antibodies to gliadin positive patients with IgA-nephropathy was pathologic in three cases (two with Marsh I) . One patient with chronic glomerulnephritis also had Marsh I.
  
  
  CONCLUSIONS
  We found no increased frequency of verified coeliac disease in 89 patients with IgA-nephropathy. Two patients with IgA-nephropathy and one patient with chronic glomerulonephritis with IgA deposits in the kidney biopsy had a Marsh I histopathology. The findings suggest a possible link of celiac disease to IgA-nephropathy and a role for antibodies to food antigens in this disorder.
authors.affiliation: Department of Neurology, University Hospital of Linköping, Linköping, Sweden. gabriel.almroth@lio.se
authors.forename: G
authors.initials: G
authors.lastname: Almroth
authors.forename: T
authors.initials: T
authors.lastname: Axelsson
authors.forename: E
authors.initials: E
authors.lastname: Müssener
authors.forename: E
authors.initials: E
authors.lastname: Grodzinsky
authors.forename: G
authors.initials: G
authors.lastname: Midhagen
authors.forename: P
authors.initials: P
authors.lastname: Olcén
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood; D002446:Celiac Disease / Q000150:complications / Q000276:immunology / Q000473:pathology; D004386:Duodenum / Q000276:immunology* / Q000473:pathology*; D005260:Female; D019204:GTP-Binding Proteins; D005903:Gliadin / Q000276:immunology*; D005922:Glomerulonephritis, IGA / Q000150:complications / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood*; D008297:Male; D008875:Middle Aged; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases / Q000276:immunology
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D005903:Gliadin; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins