The American Journal of Medicine
Volume 76, Issue 6 , Pages 1006-1012, June 1984

Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs:

Immunologic characterization of the inflammatory infiltrate

  • Walter L. Bender, M.D.

      Affiliations

    • Corresponding Author InformationCurrent address and address for reprint requests: Department of Medicine, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21205.
    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • ,
  • Andrew Whelton, M.D.

      Affiliations

    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • ,
  • William E. Beschorner, M.D.

      Affiliations

    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • ,
  • Mamdouh O. Darwish, M.D.

      Affiliations

    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • ,
  • Mary Hall-Craggs, M.D.

      Affiliations

    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
    • Current address: Department of Pathology, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201.
  • ,
  • Kim Solez, M.D.

      Affiliations

    • From the Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
    • Dr. Solez is a recipient of United States Public Health Service Research Career Development Award AM-00835.

Baltimore, Maryland USA

Accepted 2 December 1983.

Abstract 

Nine patients with the unusual combination of renal failure, nephrotic-range proteinuria, and biopsy-proved interstitial nephritis are described. Six of these patients had received nonsteroidal anti-inflammatory agents (three fenoprofen, one ibuprofen, one zomepirac, and one tolmetin). The remaining three patients had no history of exposure to drugs known to cause interstitial nephritis. Immunologic characterization of the infiltrating cells with monoclonal antibodies showed that the majority of cells in most cases were cytotoxic T cells, although some B cells were present in all cases. Giant collecting duct cells were seen In half the patients with drug exposure but in none of the others. Otherwise, there were no conspicuous morphologic differences between patients with and without drug exposure. Many of the patients had associated glomerular abnormalities. Only the zomepirac and tolmetin recipients showed pure interstitial disease. The three fenoprofen recipients and the zomepirac and tolmetin recipients regained normal renal function after the drug was discontinued. The combination of renal failure, nephrotic range proteinuria, and interstitial nephritis is one form of nephrotoxicity observed in patients treated with nonsteroidal antiinflammatory agents. However, this lesion, which may be mediated by cytotoxic T cells, may also be seen rarely in patients with no apparent drug exposure.

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 This study was supported in part by United States Public Health Service Grant AM-26809 and by a grant from Dista Products Company. Data were entered on the CLINFO computer system, supported by United States Public Health Service Grant RR35-20.

PII: 0002-9343(84)90849-0

The American Journal of Medicine
Volume 76, Issue 6 , Pages 1006-1012, June 1984