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Acute interstitial nephritis 

Acute interstitial nephritis

Chapter:
Acute interstitial nephritis
Author(s):

Simon D Roger

DOI:
10.1093/med/9780199204854.003.210901_update_002

Update:

Substantial updates throughout chapter

Inclusion of a new figure showing granuloma in AIN

New section on likely developments of the next 5-10 years

Updated further reading

Updated on 22 Sep 2016. The previous version of this content can be found here.
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date: 26 March 2017

Acute interstitial nephritis (AIN) is inflammation of the tubules and interstitium within the kidney, associated with a relatively sudden onset and a rapid decline in renal function. It is usually secondary to drugs [antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), and proton pump inhibitors being most commonly incriminated], with other causes being infections (classically streptococcal, but this is now less common) and immune disorders (systemic lupus erythematosus, sarcoidosis, and tubulointerstitial nephritis with uveitis).

Clinical features—the diagnosis of AIN should be considered in any patient with unexplained acute renal failure. Drug-induced AIN may present with a classic allergic response, including arthralgias, fever, rash, loin pain, and eosinophilia/eosinophiluria, but these are not invariable and their absence does not exclude the diagnosis. The urine typically shows low-grade proteinuria (<1 g/day). Renal biopsy is the only way to confirm or exclude the diagnosis.

Management and prognosis—treatment is by ceasing the offending agent, treating the concurrent infectious cause, or managing the immune aetiology with steroids (typically prednisolone 1 mg/kg/day, tapered to zero over 6–8 weeks). Most patients with drug-induced AIN recover renal function, but some are left with chronic renal impairment and a small proportion progress to endstage chronic kidney disease.

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