1. An atypical pattern of Epstein-Barr virus infection in a case with idiopathic tubulointerstitial nephritis.
- Author
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Okada H, Ikeda N, Kobayashi T, Inoue T, Kanno Y, Sugahara S, Nakamoto H, Yamamoto T, and Suzuki H
- Subjects
- Acute Kidney Injury etiology, Acute Kidney Injury pathology, Acute Kidney Injury virology, Aged, Herpesvirus 4, Human isolation & purification, Humans, Kidney pathology, Kidney virology, Male, Nephritis, Interstitial pathology, Nephritis, Interstitial virology, Nephrosis, Lipoid etiology, Nephrosis, Lipoid pathology, Nephrosis, Lipoid virology, T-Lymphocytes pathology, T-Lymphocytes virology, Epstein-Barr Virus Infections etiology, Nephritis, Interstitial etiology
- Abstract
Recently, Epstein-Barr virus (EBV) received attention because a latent form of its infection in renal proximal tubular epithelial cells was found to cause idiopathic, chronic tubulointerstitial nephritis. In this report, we describe the case of a patient with a replicative form of EBV infection, chronic active EBV infection (CAEBV), who developed acute tubulointerstitial nephritis and minimal change nephrotic syndrome. A renal biopsy revealed papillary infoldings of atypical tubular epithelium and adjacent dense infiltration of lymphocytes. Using in situ polymerase chain reaction methods, we detected the EBV genome in some of the infiltrating lymphocytes, but not in the tubular epithelial cells. EBV-infected T cells are thought to activate other educated T cells, as well as secrete an unrestricted variety of cytokines, thus playing a pivotal role in CAEBV and its end organ disease. Therefore, in our case, the CAEBV activated, educated T cells may have followed the EBV-infected lymphocytes as they infiltrated into the peritubular interstitium, and promoted focal tubular epithelial atypia and minimal change nephrotic syndrome. The long-term observation of such patients is important because CAEBV may progress into lymphoproliferative diseases., (Copyright 2002 S. Karger AG, Basel)
- Published
- 2002
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