Acute interstitial nephritis Acute interstitial nephritis (AIN) is an immune-mediated disorder, characterised by acute inflammation affecting the tubulo- interstitium of the kidney. It is commonly drug-induced, with proton pump inhibitors (PPIs) fast becoming the most common cause, but can be caused by other toxins, and can complicate a variety of systemic diseases and infections . Causes Clinical features The clinical presentation is typically with renal impairment but, in some patients with drug-induced AIN, there may be signs of a generalised drug hypersensitivity reaction with fever, rash and eosinophilia. Proteinuria is generally modest (PCR < 100 mg/mmol) and tubular in type . The urine may contain white blood cells and white cell casts but is sterile on culture. Eosinophils are present in up to 70% of patients but this is a non-specific finding. AIN should always be considered in patients with non-oliguric AKI. There may be a rapid deterioration of renal function in some cases of drug-induced AIN, causing the condition to be mistaken for RPGN. Investigations Renal biopsy is usually required to confirm the diagnosis . This typically shows evidence of intense inflammation, with infiltration of the tubules and interstitium by polymorphonuclear leucocytes and lymphocytes. Eosinophils may also be observed, especially in drug-induced AIN. Often granulomas may be evident, especially in drug-induced AIN or sarcoidosis . The degree of chronic inflammation in a biopsy is a useful predictor of long-term renal function. Eosinophiluria may be present but is not a good discriminator for AIN. Management Some patients with drug-induced AIN recover following withdrawal of the drug alone, but high-dose glucocoicoids (prednisolone1 mg/kg/day) may accelerate recovery and prevent long-term scarring. Other specific causes should be treated, if possible. Ref Harrison20th edition pg 278