Interstitial nephritis historical perspective: Difference between revisions
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== Historical Perspective == | == 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. | |||
* 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]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 05:33, 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.
- 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].