Display Settings:

Format

Send to:

Choose Destination
PLoS One. 2014 Apr 14;9(4):e94677. doi: 10.1371/journal.pone.0094677. eCollection 2014.

Lack of serologic evidence to link IgA nephropathy with celiac disease or immune reactivity to gluten.

Author information

  • 1Division of Digestive and Liver Diseases, Department of Medicine, Columbia University Medical Center, New York, New York, United States of America; Celiac Disease Center, Columbia University Medical Center, New York, New York, United States of America.
  • 2Division of Nephrology, Department of Medicine, Columbia University Medical Center, New York, New York, United States of America.
  • 3Esoterix, Inc., Laboratory Corporation of America Holdings, Englewood, Colorado, United States of America.
  • 4Division of Digestive and Liver Diseases, Department of Medicine, Columbia University Medical Center, New York, New York, United States of America; Celiac Disease Center, Columbia University Medical Center, New York, New York, United States of America; Institute of Human Nutrition, Columbia University Medical Center, New York, New York, United States of America.

Abstract

IgA nephropathy is the most common form of primary glomerulonephritis worldwide. Mucosal infections and food antigens, including wheat gluten, have been proposed as potential contributing environmental factors. Increased immune reactivity to gluten and/or association with celiac disease, an autoimmune disorder triggered by ingestion of gluten, have been reported in IgA nephropathy. However, studies are inconsistent about this association. We aimed to evaluate the proposed link between IgA nephropathy and celiac disease or immune reactivity to gluten by conducting a comprehensive analysis of associated serologic markers in cohorts of well-characterized patients and controls. Study participants included patients with biopsy-proven IgA nephropathy (n = 99), unaffected controls of similar age, gender, and race (n = 96), and patients with biopsy-proven celiac disease (n = 30). All serum specimens were tested for IgG and IgA antibodies to native gliadin and deamidated gliadin, as well as IgA antibody to transglutaminase 2 (TG2). Anti-TG2 antibody-positive nephropathy patients and unaffected controls were subsequently tested for IgA anti-endomysial antibody and genotyped for celiac disease-associated HLA-DQ2 and -DQ8 alleles. In comparison to unaffected controls, there was not a statistically significant increase in IgA or IgG antibody reactivity to gliadin in individuals with IgA nephropathy. In addition, the levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between IgA nephropathy patients and unaffected controls. Results of the additional anti-endomysial antibody testing and HLA genotyping were corroborative. The data from this case-control study do not reveal any evidence to suggest a significant role for celiac disease or immune reactivity to gluten in IgA nephropathy.

PMID:
24732864
[PubMed - in process]
PMCID:
PMC3986214
Free PMC Article

Images from this publication.See all images (3)Free text

Figure 1
Figure 2
Figure 3
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk