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Nephrol Dial Transplant (2004) 19: 8-11
© European Renal Association–European Dialysis and Transplant Association

Editorial Comment

The changing profile of acute tubulointerstitial nephritis

Richard J. Baker1 and Charles D. Pusey2

1Renal Unit, St James University Hospital, Beckett Street, Leeds and 2Renal Section, Division of Medicine, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, UK

Correspondence and offprint requests to: Dr Richard Baker, Renal Unit, St James University Hospital, Beckett Street, Leeds LS9 7TF, UK. Email: richard.baker@leedsth.nhs.uk

Keywords: acute renal failure; acute tubulointerstitial nephritis; steroids; tubulointerstitial nephritis and uveitis syndrome

The first 150 words of the full text of this article appear below.



   Introduction
 
‘Cellular and fluid exudation in the interstitial tissue...’ was described by Councilman in 1898 when he examined the kidneys of patients dying of scarlet fever and diptheria [1]. In particular he noted that the organs were sterile thus raising the possibility of an allergic-type phenomenon. This entity was termed acute tubulointerstitial nephritis (ATIN). 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 aetiology is presumed to be immune-mediated [2]. This is illustrated by the rapid recrudescence of disease upon inadvertent rechallenge in . . . [Full Text of this Article]



   Prevalence and clinical picture
 


   Diagnosis
 


   Aetiology
 


   TINU syndrome
 


   Outcome and prognostic factors
 


   Steroid treatment or not?
 


   Conclusion
 

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