Medikamenteninduzierte akute interstitielle nephritis

Acute interstitial nephritis is a frequent cause of acute kidney injury. The etiology of this disease includes drug-induced, ideopathic, infectious or autoimmun/systemic forms. In 60-70% drug-induced acute interstitial nephritis is the commonest etiology. The first major discription about drug-induced acute interstitial nephritis was published by Baldwin et al. [2] in 1968, naming Methicillin as causing agent. Since then, many further agents from different drug-classes have been recognized. The majority of cases have been caused by antimicrobial agents and nonsteroidal anti-inflammatory drugs. The pathogenesis of drug-induced acute interstitial nephritis most likely involves an allergic response to endogenous renal or non-renal antigens. A definitive diagnosis of acute interstitial nephritis requires a renal biopsy. The histopathological investigation shows characteristic inflammatory cell infiltrates, tubulitis, interstitial edema and eventually interstital fibrosis or granuloma. The clinical presentation and laboratory findings are variable and depend on the class of drugs involved. Acute kidney injury is often accompanied by extrarenal symptoms as fever, skin rashes, arthralgias and eosinophilia. The mainstay of treatment is the identification and removal of the causing agent. An early initiated corticosteroid therapy seems to approve the recovery of renal function and appears to prevent chronic renal impairment. The prognosis of drug-induced acute interstitial nephritis is generally good, provided that the disease is regonignized and treated at an early stage.