The possible involvement of intestine-derived IgA1: a case of IgA nephropathy associated with Crohn’s disease


Background:
A link between IgA nephropathy and Crohn’s disease has recently been reported. Other researchers hypothesize that intestine-derived IgA complexes deposit in glomerular mesangial cells, eliciting IgA nephropathy. Intestinal mucosal plasma cells mainly secrete IgA2. Nevertheless, IgA1 deposition is strongly implicated as being the primary cause of IgA nephropathy.

Case presentation:
A 46-year-old Japanese man developed IgA nephropathy 29 years ago, following tonsillectomy. As a result, a normal urinalysis was obtained. The patient previously suffered Crohn’s disease followed by urinary occult blood and proteinuria six years ago. Exacerbation of IgA nephropathy was highly suspected. Therefore a renal biopsy was performed. A diagnosis of exacerbation of IgA nephropathy with mesangial cell proliferation and fibrotic cellular crescent was based upon the pathological findings. The patient exhibited a positive clinical course and eventually achieved a remission with immunosuppressive therapy including prednisolone treatment. Immunostaining for the detection of IgA subtypes was performed on both of his kidney and excised ileum. The results revealed IgA1 and IgA2 deposition by submucosal cells in intestine. Furthermore, IgA1 deposition of mesangial areas in the patient’s kidney, indicated an association of IgA1with the exacerbation of IgA nephropathy.

Conclusion:
This case represents the possibility that the intestine-derived IgA1 can be the origin of galactose-deficient IgA which is known to cause IgA nephropathy exacerbation.

Keywords:
Crohn’s disease, IgA nephropathy, IgA1, IgA2, Inflammatory bowel disease


Autoři: Tomohiro Terasaka 1;  Haruhito A. Uchida 1,2*;  Ryoko Umebayashi 1;  Keiko Tsukamoto 1;  Keiko Tanaka 1;  Masashi Kitagawa 1;  Hitoshi Sugiyama 1,3;  Hiroaki Tanioka 4;  Jun Wada 1
Působiště autorů: Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, -5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan. 1;  Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan. 2;  Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan. 3;  Department of Medicine Oncology, Okayama Rosai Hospital, 1-10-25 Chikkomidori-machi, Minami-ku, Okayama 702-8055, Japan. 4
Vyšlo v časopise: BMC Nefrol 2016, 17:122
Kategorie: Case report
prolekare.web.journal.doi_sk: 10.1186/s12882-016-0344-1

© 2016 The Author(s).

Open access
This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
The electronic version of this article is the complete one and can be found online at: http://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-016-0344-1

Souhrn

Background:
A link between IgA nephropathy and Crohn’s disease has recently been reported. Other researchers hypothesize that intestine-derived IgA complexes deposit in glomerular mesangial cells, eliciting IgA nephropathy. Intestinal mucosal plasma cells mainly secrete IgA2. Nevertheless, IgA1 deposition is strongly implicated as being the primary cause of IgA nephropathy.

Case presentation:
A 46-year-old Japanese man developed IgA nephropathy 29 years ago, following tonsillectomy. As a result, a normal urinalysis was obtained. The patient previously suffered Crohn’s disease followed by urinary occult blood and proteinuria six years ago. Exacerbation of IgA nephropathy was highly suspected. Therefore a renal biopsy was performed. A diagnosis of exacerbation of IgA nephropathy with mesangial cell proliferation and fibrotic cellular crescent was based upon the pathological findings. The patient exhibited a positive clinical course and eventually achieved a remission with immunosuppressive therapy including prednisolone treatment. Immunostaining for the detection of IgA subtypes was performed on both of his kidney and excised ileum. The results revealed IgA1 and IgA2 deposition by submucosal cells in intestine. Furthermore, IgA1 deposition of mesangial areas in the patient’s kidney, indicated an association of IgA1with the exacerbation of IgA nephropathy.

Conclusion:
This case represents the possibility that the intestine-derived IgA1 can be the origin of galactose-deficient IgA which is known to cause IgA nephropathy exacerbation.

Keywords:
Crohn’s disease, IgA nephropathy, IgA1, IgA2, Inflammatory bowel disease


Zdroje

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16. Maté-Jimenez J, et al. Tonsillectomy and inflammatory bowel disease location. Eur J Gastroenterol Hepatol. 1996;8:1185–8.

17. Filiopoulos V, et al. IgA nephropathy in association with Crohn’s disease: a case report and brief review of the literature. Ren Fail. 2010;32:523–7.

18. Hiki Y, et al. Underglycosylation of IgA1 hinge plays a certain role for its glomerular deposition in IgA nephropathy. J Am Soc Nephrol. 1999;10:760–9.

19. Tomana M, et al. Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies. J Clin Invest. 1999;104:73–81.

20. Kett K, et al. Local IgA subclass alterations in ulcerative colitis and Crohn’s disease of the colon. Gut. 1987;28:1013–21.

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Detská nefrológia Nefrológia
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