PRESENTATION AND DIAGNOSIS

Acute interstitial nephritis typically manifests as AKI following the recent introduction of a new medication. Eighty percent of patients develop symptoms within 3 weeks of drug introduction, although there can be a latent period of several months following onset of NSAID use. The AKI can manifest either as oliguria or as an asymptomatic elevation in serum creatinine concentration noted on routine serum chemistries. In classic descriptions, the renal injury is accompanied by the triad of fever, rash, and eosinophilia; however, this picture emerged when the major pathogenetic agent was methicillin, which often triggered a hypersensitivity-type reaction. At present, largely because of the growing incidence of NSAID-related AIN, allergic symptoms are less consistent. Fever, rash, and eosinophilia are each seen in about 15% to 25% of patients, and the entire triad is seen in only 10%. In addition to these variable allergic symptoms, a fraction of patients may experience fank pain, gross hematuria, or both. Flank pain likely represents distention of the renal capsule secondary to interstitial edema. Hypertension and gross edema are uncommon.