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* In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of diphtheria and scarlet fever.<ref>Councilman WT. Acute interstitial nephritis. J Exp Med  1898; 3: 393</ref>
* In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of diphtheria and scarlet fever.<ref>Councilman WT. Acute interstitial nephritis. J Exp Med  1898; 3: 393</ref>
* He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics.
* He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics.
* The widespread introduction of percutaneous renal biopsy led to the discovery of similar findings in association with drug-related renal failure, in particular related to the use of penicillins and sulphonamides. Histological examination in ATIN reveals an infiltrate, which is largely composed of T cells, together with some macrophages and plasma cells. As there is some evidence for cutaneous delayed-type hypersensitivity and positive ''in vitro''lymphocyte stimulation tests in response to suspected drugs, the etiology is presumed to be immune-mediated [2]. This is illustrated by the rapid recrudescence of disease upon inadvertent rechallenge in drug-related ATIN, a clear manifestation of an immunological memory response [3–5].
* The widespread introduction of percutaneous renal biopsy led to the discovery of similar findings in association with drug-related renal failure, in particular related to the use of penicillins and sulphonamides. Histological examination in ATIN reveals an infiltrate, which is largely composed of T cells, together with some macrophages and plasma cells. As there is some evidence for cutaneous delayed-type hypersensitivity and positive ''in vitro''lymphocyte stimulation tests in response to suspected drugs, the etiology is presumed to be immune-mediated <ref>Kelly C, Tomaszewski J, Neilson E. Immunopathogenic mechanisms of tubulointerstitial injury. In: Tisher C, Brenner B, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn., Vol. 1. J. B. Lippincott & Co, Philadelphia, PA, 1994; 699–722</ref>. This is illustrated by the rapid recrudescence of disease upon inadvertent rechallenge in drug-related ATIN, a clear manifestation of an immunological memory response [3–5].


==References==
==References==

Revision as of 05:40, 19 July 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [[1]]; Associate Editor(s)-in-Chief:Mohsen Basiri M.D.

Overview

Historical Perspective

  • In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of diphtheria and scarlet fever.[1]
  • He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics.
  • The widespread introduction of percutaneous renal biopsy led to the discovery of similar findings in association with drug-related renal failure, in particular related to the use of penicillins and sulphonamides. Histological examination in ATIN reveals an infiltrate, which is largely composed of T cells, together with some macrophages and plasma cells. As there is some evidence for cutaneous delayed-type hypersensitivity and positive in vitrolymphocyte stimulation tests in response to suspected drugs, the etiology is presumed to be immune-mediated [2]. This is illustrated by the rapid recrudescence of disease upon inadvertent rechallenge in drug-related ATIN, a clear manifestation of an immunological memory response [3–5].

References

  1. Councilman WT. Acute interstitial nephritis. J Exp Med 1898; 3: 393
  2. Kelly C, Tomaszewski J, Neilson E. Immunopathogenic mechanisms of tubulointerstitial injury. In: Tisher C, Brenner B, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn., Vol. 1. J. B. Lippincott & Co, Philadelphia, PA, 1994; 699–722

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