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Kidney Week

Abstract: PO1796

IgA Nephropathy Complicated with Crohn Disease: A Clinical and Pathological Study of Kidney Biopsied Cases

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Akiyama, Minako, Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Kousuke, Shimomura, Tokyo Yamate Medical Center, Shinjuku-ku, Tokyo, Japan
  • Yoshimoto, Shaho, Tokyo Yamate Medical Center, Shinjuku-ku, Tokyo, Japan
  • Sako, Minako, Tokyo Yamate Medical Center, Shinjuku-ku, Tokyo, Japan
  • Kodama, Makoto, Tokyo Yamate Medical Center, Shinjuku-ku, Tokyo, Japan
  • Abe, Keiko, Tokyo Yamate Medical Center, Shinjuku-ku, Tokyo, Japan
  • Sano, Mariko, Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Kang, Dedong, Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Takaki, Takashi, Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Wada, Yukihiro, Division of Nephrology, Department of Medicine, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Iyoda, Masayuki, Department of Microbiology and Immunology, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
  • Honda, Kazuho, Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo, Japan
Background

Intestinal immunity is closely related with the pathogenesis and progression of renal diseases, called as “entero-renal linkage”. To figure out the association between IgA nephropathy (IgAN) and Crohn's disease (CD), we performed the clinico-pathological study of IgAN patients with (CD-IgAN) and without CD (NOS-IgAN).

Methods

We enrolled 29 patients diagnosed with IgAN by renal biopsy in Tokyo Yamate Medical Center from 2009 to 2017. The patients were divided into CD-IgAN (n=18) and NOS-IgAN (n=11) and investigated their clinical and pathological findings. IgA subclasses and galactose-deficient IgA1 (Gd-IgA1) on glomerulus were examined by immunohistochemistry.

Results

No significant difference in the grades of urinary protein and hematuria was observed between CD-IgAN and NOS-IgAN, but CD-IgAN had elevated serum creatinine (sCr) and lower rate in clinical remission after steroid treatment as compared to NOS-IgAN. Pathologically, CD-IgAN had remarkably higher levels of global glomerulosclerosis (%), grades of interstitial fibrosis and tubular atrophy (IF/TA) than NOS-IgAN. Immunohistochemically, IgA1 was a dominant subclass and Gd-IgA1 was frequently detected in glomerular mesangium in both groups. No difference was noted in the extents of IgA1, IgA2 and Gd-IgA1 deposition, depending on the presence or absence of CD.

Conclusion

From the results of the subclasses and galactose-deficiency of the IgA molecules, no difference was suggested in the etiology and pathogenesis between CD-IgAN and NOS-IgAN. However, advanced glomerular sclerosis and tubulointerstitial fibrosis in renal pathology and highly resistant clinical features to medical treatments in CD-IgAN suggest that the intestinal immunity and other clinical factors associated with CD may promote and activate the inflammatory process of IgAN.