Interstitial nephritis historical perspective: Difference between revisions
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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 <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 | * 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.<ref> Pusey CD, Saltissi D, Bloodworth L, Rainford DJ, Christie JL. Drug associated acute interstitial nephritis: clinical and pathological features and the response to high dose steroid therapy. Q J Med 1983; 52: 194–211</ref>Saltissi D, Pusey CD, Rainford DJ. Recurrent acute renal failure due to antibiotic-induced interstitial nephritis. Br Med J 1979; 1: 1182–1183<ref></ref><ref>Sloth K, Thomsen AC. Acute renal insufficiency during treatment with azathioprine. Acta Med Scand 1971; 189: 145–148</ref> | ||
==References== | ==References== | ||
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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]Saltissi D, Pusey CD, Rainford DJ. Recurrent acute renal failure due to antibiotic-induced interstitial nephritis. Br Med J 1979; 1: 1182–1183[4]
References
- ↑ Councilman WT. Acute interstitial nephritis. J Exp Med 1898; 3: 393
- ↑ 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
- ↑ Pusey CD, Saltissi D, Bloodworth L, Rainford DJ, Christie JL. Drug associated acute interstitial nephritis: clinical and pathological features and the response to high dose steroid therapy. Q J Med 1983; 52: 194–211
- ↑ Sloth K, Thomsen AC. Acute renal insufficiency during treatment with azathioprine. Acta Med Scand 1971; 189: 145–148