Praga M, Sevillano A, Aunon, Pilar, Gonzalez E. Changes in the aetiology, clinical presentation and management of acute interstitial nephritis, an increasingly common cause of acute kidney injury. NDT 2014 Oct 16 [Epub ahead of print]. PMID: 25324356
Jelakovic B, Nikolic J, Radovanovic Z, et al. Consensus statement on screening, diagnosis, classification and treatment of endemic (Balkan) nephropathy. Nephrol Dial Transplant. 2013 Oct 28. [Epub ahead of print] PMID: 24166461.
Braden GL, O’Shea MH, Mulhern JG. Tubulointerstitial diseases. Am J Kidney Dis 2005. Sep;46(3):560-72. Review. PMID: 16129220.
Definition and EtiologyTop
Interstitial nephritis is characterized by inflammation of the renal interstitium. It may be secondary to glomerular or renal vascular damage and usually coexists with renal tubular damage, which is why it is often termed tubulointerstitial nephritis (TIN).
Acute interstitial nephritis (AIN) is associated with acute kidney injury (AKI), which develops over a period of days to several weeks and is often reversible. Most often AIN is an immunologically induced hypersensitivity reaction to an antigen (most commonly a drug or an infectious agent).
Chronic interstitial nephritis (CIN) develops over months or years and is associated with progressive fibrosis of the tubulointerstitium, leading to chronic kidney disease. Tubulointerstitial injury can be caused by exogenous or endogenous toxins, infections, immune-mediated mechanisms, obstruction, or ischemia.