Allergic and Drug-Induced Interstitial Nephritis

Excerpt

Drug-induced acute interstitial nephritis (DI-AIN), also called allergic acute interstitial nephritis, is the most common cause of acute interstitial nephritis (AIN) in developed countries. DI-AIN is associated with a sharp decline in renal function, often requiring dialysis, and has the potential for permanent renal insufficiency, especially if left untreated. Differentiating from other causes of acute kidney injury and discontinuing the causative medication is key to early reversibility.

Interstitial nephritis was first described in 1898 by William Thomas Councilman, chief pathologist at Brigham Hospital, who noted nonsuppurative interstitial lesions on autopsies of patients with streptococcal infections, and this term is used to describe various immune-mediated kidney disorders that cause significant inflammatory cell infiltration of the renal interstitium and tubules while sparing the glomeruli.

The most common form of AIN in developed countries is caused by drug exposure, estimated at 70% to 75% of cases. DI-AIN is a frequent causative agent of acute kidney injury (AKI), responsible for about 20% of renal biopsies performed for unexplained AKI. AIN is associated with an acute decline in renal function and may progress to permanent renal insufficiency or even end-stage renal disease (ESRD). AIN has been defined as an increase of 0.5 mg/dL or 50% in serum creatinine over a 24- to 72-hour period starting 24 to 48 hours after exposure to a potential triggering medication.

The classic clinical presentation of AIN characterized by fever, rash, and eosinophilia was prominently associated with methicillin use, which occurred in about 17% of cases. However, this specific presentation is less common with other medications known to cause AIN. Identification and discontinuation of the offending medication are the mainstays of treatment, with conflicting evidence regarding the benefit of steroid treatment. With early recognition and proper treatment, AIN and its associated renal failure are generally reversible.

For information on other causes of interstitial nephritis (genetic, idiopathic, infectious, immune-mediated, and associated with various systemic inflammatory disorders), as well as anti-tubular basement membrane disease and tubulointerstitial nephritis and uveitis syndrome (TINU), see our companion StatPearls reference article on Tubulointerstitial Nephritis. Autosomal dominant tubulointerstitial kidney disease is also described elsewhere.