Inflammation Lesions in Kidney Transplant Biopsies: Association with Survival Is Due to the Underlying Diseases

Authors

  • J. Sellarés,

    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Medicine, Division of Nephrology and Transplant Immunology, University of Alberta, Edmonton, AB, Canada
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  • D. G. de Freitas,

    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Medicine, Division of Nephrology and Transplant Immunology, University of Alberta, Edmonton, AB, Canada
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  • M. Mengel,

    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada
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  • B. Sis,

    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada
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  • L. G. Hidalgo,

    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Medicine, Division of Nephrology and Transplant Immunology, University of Alberta, Edmonton, AB, Canada
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  • A. J. Matas,

    1. Department of Surgery, University of Minnesota, Minneapolis, MN
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  • B. Kaplan,

    1. Department of Medicine (Division of Nephrology), University of Arizona, Tucson, AZ
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  • P. F. Halloran

    Corresponding author
    1. Alberta Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada
    2. Department of Medicine, Division of Nephrology and Transplant Immunology, University of Alberta, Edmonton, AB, Canada
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Corresponding author: Philip F. Halloran, Phil.halloran@ualberta.ca

Abstract

Assessment of kidney transplant biopsies relies on nonspecific inflammatory lesions: Interstitial infiltrates (i), tubulitis (t) and intimal arteritis (v). We studied the relationship between inflammation and prognosis in biopsies for clinical indications from 314 patients (median follow-up 25 months). We used a modified Banff classification, separately assessing inflammation (i-) in nonscarred (i-Banff), scarred (i-IFTA) and whole cortex (i-total), plus tubulitis and intimal arteritis. In early biopsies (<1 year), i- and t-lesions had no association with graft survival. In late (>1 year) biopsies, all i-scores correlated with progression to failure, due to the association of these infiltrates with progressive diseases: antibody-mediated rejection (ABMR) and glomerulonephritis. Tubulitis in nonscarred areas had no impact on survival. Severe tubulitis including scarred areas (tis3) was associated with worse survival, but reflected polyoma virus nephropathy or ABMR, not T-cell-mediated rejection. Intimal arteritis (v-lesions) had no association with allograft loss in early or late biopsies. In multivariate analysis, outcome was better predicted by the presence of progressive disease than by inflammation. Thus inflammation in late kidney transplants has no inherent prognostic impact, but predicts reduced survival because inflammation indicates actively progressing diseases. The most important predictor of outcome is the diagnosis of a progressive disease.

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