Factors related to renal cortical atrophy development after glucocorticoid therapy in IgG4-related kidney disease: a retrospective multicenter study View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11-25

AUTHORS

Ichiro Mizushima, Motohisa Yamamoto, Dai Inoue, Shinichi Nishi, Yoshinori Taniguchi, Yoshifumi Ubara, Shoko Matsui, Tetsuhiko Yasuno, Hitoshi Nakashima, Hiroki Takahashi, Kazunori Yamada, Hideki Nomura, Masakazu Yamagishi, Takao Saito, Mitsuhiro Kawano

ABSTRACT

BackgroundIn immunoglobulin G4-related kidney disease (IgG4-RKD), focal or diffuse renal cortical atrophy is often observed in the clinical course after glucocorticoid therapy. This study aimed to clarify the factors related to renal atrophy after glucocorticoid therapy in IgG4-RKD.MethodsWe retrospectively evaluated clinical features including laboratory data and computed tomography (CT) findings before and after glucocorticoid therapy in 23 patients diagnosed with IgG4-RKD, all of whom were followed up for more than 24 months.ResultsSeventeen patients were men, and six were women (average age 62.0 years). Average follow-up period was 54.9 months. The average estimated glomerular filtration rate (eGFR) at diagnosis was 81.7 mL/min/1.73 m2. All patients had had multiple low-density lesions on contrast-enhanced CT before glucocorticoid therapy, and showed disappearance or reduction of these lesions after it. Pre-treatment eGFR and serum IgE level in 11 patients in whom renal cortical atrophy developed 24 months after the start of glucocorticoid therapy were significantly different from those in 12 patients in whom no obvious atrophy was found at that time (68.9 ± 30.1 vs 93.5 ± 14.1 mL/min/1.73 m2, P = 0.036, and 587 ± 254 vs 284 ± 263 IU/mL, P = 0.008, respectively). Pre-treatment eGFR and serum IgE level were also significant risk factors for renal atrophy development 24 months after the start of therapy with an odds ratio of 0.520 (per 10 mL/min/1.73 m2, 95% confidence interval (CI) 0.273–0.993, P = 0.048) and 1.090 (per 10 IU/mL, 95% CI: 1.013–1.174, P = 0.022), respectively, in age-adjusted, sex-adjusted, serum IgG4 level-adjusted logistic regression analysis. Receiver operating characteristic curve analysis showed that eGFR of less than 71.0 mL/min/1.73 m2 and serum IgE of more than 436.5 IU/mL were the most appropriate cutoffs and yielded sensitivity of 63.6% and specificity of 100%, and sensitivity of 90.9% and specificity of 75.0%, respectively, in predicting renal atrophy development.ConclusionsThis study suggests that pre-treatment renal insufficiency and serum IgE elevation predict renal atrophy development after glucocorticoid therapy in IgG4-RKD. More... »

PAGES

273

References to SciGraph publications

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  • Journal

    TITLE

    Arthritis Research & Therapy

    ISSUE

    1

    VOLUME

    18

    Author Affiliations

  • Division of Nephrology and Rheumatology, Department of Internal Medicine, Ishikawa Prefectural Central Hospital, Kanazawa, Japan
  • The First Department of Internal Medicine, Sapporo Medical University, South 1, West 16, Chuo-ku, 060-8543, Sapporo, Hokkaido, Japan
  • Department of Radiology, Kanazawa University Graduate School of Medical Science, 13-1 Takara-machi, 920-8640, Kanazawa, Ishikawa, Japan
  • Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki, Chuo-ku, 650-0017, Kobe, Hyogo, Japan
  • Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, 783-8505, Nankoku, Kochi, Japan
  • Nephrology Center and Okinaka Memorial Institute for Medical Research, Toranomon Hospital, Toranomon 2-2-2, Minato-ku, 105-8470, Tokyo, Japan
  • Health Administration Center, University of Toyama, 2630 Sugitani, 930-0194, Toyama-shi, Toyama, Japan
  • Division of Nephrology and Rheumatology, Department of Internal Medicine, Fukuoka University, 7-45-1, Nanakuma, 814-0180, Jonan-ku, Fukuoka, Japan
  • Division of Rheumatology, Department of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, 920-8640, Kanazawa, Ishikawa, Japan
  • Department of General Medicine, Kanazawa University Hospital, 13-1 Takara-machi, 920-8640, Kanazawa, Ishikawa, Japan
  • Division of Cardiology, Department of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medicine, 13-1 Takara-machi, 920-8640, Kanazawa, Ishikawa, Japan
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s13075-016-1175-y

    DOI

    http://dx.doi.org/10.1186/s13075-016-1175-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1029613040

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27884179


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