Acute interstitial nephritis (AIN) is a kidney lesion typically causes decline of kidney function. Characterized by the presence of inflammatory infiltrates and edema within the interstitium, it is most often induced by drug therapy. When the classic findings of rash, fever, and eosinophilia are present with history of culprit drug administration, diagnosis of AIN is usually obvious and kidney biopsy often considered unnecessary. Of many drugs associated with AIN, nonsteroidal anti-inflammatory drugs (NSAIDs) are the ones of most concern. Their mechanism of action which are associated with the enzymes of arachidonic acid (cyclooxygenases: COX-1 and COX-2) and formation of prostanoids (prostaglandins, prostacyclins, and thromboxanes), may affects various structures of the human body including the kidneys. We reported a case of 29-years-old male presented with fever and rash, accompanied with dyspnea and reduced urine production. He had history of regular mefenamic acid consumption for the last 8 months due to on-off toothache. Physical examination showed the fever of 380C, tachypnea, pulmonary crackles, bilateral pre-tibial edema, and generalized maculopapular rash. Laboratory results revealed eosinophilia (34%), hyperkalemia (6.8 mEq/L), high urea level (299 mg/dL), elevated creatinine (10.5 mg/dL), and pyuria with cylinder granular casts on urinalysis. These results suggested diagnosis of AIN, therefore we start him on intravenous methylprednisolone 32.5 mg twice a day. Supportive dialysis on the first and third day of admission was given due to hyperkalemia and deleterious kidney function. Following treatment, his condition improved and he was discharge with creatinine level of 1.8 mg/dL. The patient was then followed-up at the outpatient clinic, he reported no other symptoms, skin rashes were resolved, and serum creatinine was back to the normal level of 1.0 mg/dL.