Interstitial nephritis is seen with all except
Acute interstitial nephritis Acute interstitial nephritis (AIN) is an immune-mediated disorder, characterised by acute inflammation affecting the tubulointerstitium 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 . 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. Chronic interstitial nephritis Chronic interstitial nephritis (CIN) is characterised by renal dysfunction with fibrosis and infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages, in association with tubular damage Pathophysiology This disease may follow on from AIN that does not resolve, or may be associated with ingestion of various toxins and drugs, or with metabolic and chronic inflammatory diseases . In many patients, CIN presents at a late stage and no underlying cause can be identified. Genetic causes may underlie many of these cases . Toxins that have been associated with CIN include those contained within the plant Aristolochia clematitis (bihwo). These are probably responsible for the severe nephrotoxicity that can be associated with treatment with herbal medicines in Asia and for Balkan nephropathy, which affects isolated rural communities in Bosnia, Bulgaria, Croatia, Romania and Serbia, possibly through contaminated flour. The nephropathy is commonly linked with tumours of the collecting system and is probably due to the mutagenic effects of the plant toxin on the urothelial epithelium. Ingestion of mushrooms within the Coinarius genus can cause a devastating and irreversible renal tubular toxicity. It is encountered occasionally in Scandina and Scotland. Ref Harrison20th edition pg 278
Beta lactam inhibitors
INH
Diuretics
Allopurinol
Kidney