LAUSR

Medications are the most common cause of AIN in adults, although large-scale epidemiological data in paediatrics are lacking [1–4]. A host of different drugs have been implicated in AIN including antibiotics (particularly β-lactams), nonsteroidal antiinflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), diuretics and anti-epileptic drugs [5–8]. The onset of renal involvementmay be acute over the course of hours to days butmay also be insidious over several months. Typical presentation is within 2–3 weeks of exposure to a drug, but this may depend on dose and duration of administration [9]. Hypersensitivity reactions may occur with pyrexia, rash and eosinophilia. These reactions are more common with penicillin-induced AIN and much rarer in NSAID-induced disease [9]. Rifampicin has been linked with a unique, severe presentation of AINwith features of acute tubular necrosis on biopsy [10, 11]. There remains a lack of understanding as to the individual risk factors that predispose to drug-induced tubulointerstitial injury. Infective causes of AIN may be bacterial, viral, fungal or parasitic. The nature of renal parenchymal inflammation may either be by direct invasion into the tissues or by an immunologically mediated ‘reactive’ inflammatory process. Prior to widespread antibiotic availability, group A streptococcal (GAS) AIN was reported on post-mortem biopsies in a large number of children with scarlet fever [12]. GAS continues to be a relatively common bacterial cause of AIN. Other bacterial causes include Mycobacterium tuberculosis, Mycoplasma pneumoniae, Yersinia spp. and Leptospira spp. [13–15]. Adenovirus has been linked with necrotising AIN in bone marrow transplant recipients [16, 17], and AIN accounts for around a quarter of renal disease in patients with human immunodeficiency virus (HIV), although many of these cases may be secondary to medications, or infectious agents due to underlying immunodeficiency [18]. Following renal transplant, cytomegalovirus (CMV), polyoma (BK) virus and JC virus have all been linked with AIN and an increased risk of graft dysfunction [19, 20]. Other viral causes of AIN include the hantavirus family. Fungal causes of AIN include histoplasmosis [21], and parasitic causes include malaria [22]. Systemic immunological disorders may be associated with AIN with or without glomerulonephritis: