To determine the risk of future biopsy-verified IgA nephropathy (IgAN) among individuals with biopsy-verified celiac disease (CD).
Individuals with CD suffer increased risk of end-stage renal disease. An association between CD and IgAN has been suggested; however, results have been inconclusive and no previous study has considered the risk of IgAN in biopsy-verified CD.
We performed a population-based prospective cohort study. We identified 27,160 individuals with CD (Marsh stage III) and no previous renal disease through small-intestinal biopsy reports obtained between July 1969 and February 2008 in all (n=28) Swedish pathology departments. Individuals with IgAN were identified by biopsy reports acquired at the 4 Swedish pathology departments specialized in renal pathology. Cox regression analysis was used to determine the risk of future IgAN among individuals with CD compared with 133,949 age-matched and sex-matched reference individuals.
Seven (0.026%) individuals with CD and 11 (0.008%) reference individuals developed IgAN. We found an increased risk of biopsy-verified IgAN among individuals with CD [hazard ratio, 3.03; 95% confidence interval, 1.22-7.56]. The risk increase remained statistically significant after adjustment for prior liver disease and country of birth.
Individuals with CD suffer a 3-fold increased risk of future IgAN. Our findings warrant awareness of renal function in individuals with CD.
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*Clinical Epidemiology Unit, Department of Medicine
†Department of Pathology, Karolinska University Hospital, Stockholm
‡Department of Pediatrics, Örebro University Hospital, Örebro, Sweden
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Specific author contributions: A.W., main investigator, performed data collection and analysis and wrote the first draft of the manuscript; B.S., critical input regarding data collection and revision of manuscript; M.F., study concept and design, interpretation of data, critical revision of the manuscript; J.F.L., study concept and design, supervision of the study, statistical analysis, revision of the manuscript. JFL is the study guarantor.
A.W. was supported by a grant from the Karolinska Institute Board of Postgraduate education (KID). J.F.L. was supported by a grant from the Örebro University Hospital while writing this article. This project was supported by a grant from The Swedish Society of Medicine, the Swedish Research Council, the Sven Jerring Foundation, the Örebro Society of Medicine, the Karolinska Institutet, the Clas Groschinsky Foundation, the Juhlin Foundation, the Majblomman Foundation, and the Swedish Celiac Society.
The authors declare that they have nothing to disclose.
Reprints: Adina Welander, MD, PhD, Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, 17176 Stockholm, Sweden (e-mail: firstname.lastname@example.org).
Received July 26, 2012
Accepted December 21, 2012