The case: A 57-year-old man presented to hospital with a 2-week history of progressive malaise, myalgia, fever, nausea, vomiting, diarrhea, polyuria and polydipsia. He had a history of gastresophageal reflux that did not respond to ranitidine. He had started taking oral pantoprazole (40 mg daily) 6 weeks earlier. The patient had a history of coronary artery disease and was taking acetylsalicylic acid (81 mg daily) and atorvastatin (40 mg daily). He reported having taken ibuprofen (400 mg) for myalgia no more than 3 times over the 2-week period before presentation. He had no history of renal disease or drug allergies.On presentation, the patient was afebrile (temperature 36.5°C), with a blood pressure of 127/82 mm Hg, a pulse of 72 beats/min, a respiratory rate of 18 breaths/min and an oxygen saturation of 97% in room air. The jugular venous pressure was measured at the sternal angle. His chest sounds were normal, and there was no pericardial friction rub or peripheral edema. The results of a dermatological examination were unremarkable.The results of laboratory tests are listed in Table 1. Of note, the patient had a serum creatinine level of 300 (normal 53-106) μmol/L. Two years ago, his creatinine level had been 100 μmol/L. He had mild hyperkalemia, but his electrolyte levels were otherwise normal. His leukocyte and eosinophil counts were normal. The ratio of protein to creatinine in his urine was 28 (normal 0-23), and the protein level in a 24-hour urine collection was 410 (normal < 150) mg. Protein electrophoresis showed that the protein in the urine was predominantly albumin. When analyzed by use of Wright stain, the first urine sample was negative for eosinophils, but 1% of the leukocytes in the second sample were eosinophils.Treatment included volume repletion and discontinuation of pantoprazole. Ultrasonography showed that both of the patient's kidneys were of normal size, and that there was normal echogenicity with no hydronephrosis. Over the next 4 days, his creatinine level decreased to 235 μmol/L. A needle core biopsy of 1 of the patient's kidneys was performed on day 6. The biopsy was indicated because the patient had ongoing acute renal failure with major proteinuria for which pre-and post-renal causes had been ruled out (there had been very minor improvement with volume repletion and the results of a renal ultrasound were normal). The biopsy showed moderate-to-severe patchy interstitial infiltrates, predominantly plasma cells with some lymphocytes and occasional eosinophils (Figure 1). Immunoflourescence was negative for IgG, IgA, IgM, C3, C1q and fibrin antibodies. These results supported the diagnosis of acute interstitial nephritis.