Introduction Acute interstitial nephritis (AIN), also called tubulointerstitial nephritis, is a renal pathology that can cause a significant decline in kidney function. Drug-induced AIN accounts for 70% of all cases and is often due to non-steroidal anti-inflammatory drugs (NSAIDs), antimicrobials, and proton pump inhibitors. However, there have been isolated reports of other drugs being responsible for AIN. We hereby report a case of furosemide-induced AIN. Case Presentation A 68-year-old caucasian male with a medical history significant for chronic kidney disease (CKD) stage 3 due to hypertensive nephrosclerosis with a baseline serum creatinine (Cr) of 1.3-1.5, hypertension, hyperlipidemia, atrial fibrillation, heart failure with preserved ejection fraction (HFpEF), and hypogonadism was admitted for evaluation of worsening renal failure. At initial evaluation, the patient had nonspecific symptoms like malaise, nausea, and vomiting but denied any other complaints. Physical examination was unremarkable, without any rashes or abdominal bruit. The patient’s creatinine progressively trended up from his baseline to 3.5 over three months. Pre-renal pathology was suspected initially, and the patient's furosemide was held on admission with concurrent fluid resuscitation. However, this did not improve his kidney function as repeat lab work showed a worsening Cr level of 4.4, along with a blood urea nitrogen (BUN) of 72. Further evaluation showed a complete blood count significant for mild eosinophilia with urinalysis revealing hematuria, pyuria with eosinophiluria but no protein, WBC casts, or RBC casts. Renal ultrasound and abdominal CT scan were unremarkable. The patient had no known drug allergies until that point and was on a stable medication regimen for his chronic conditions for several years, except for a daily dose of furosemide started three months ago for fluid retention and elevated BNP. Ultrasound-guided renal biopsy revealed findings consistent with acute interstitial nephritis on top of chronic tubulointerstitial fibrosis plus underlying moderate arterial sclerosis from hypertension. Other extensive workup was negative for any autoimmune process, IgG4 related disease, sarcoidosis, or infection, thus favoring the diagnosis of drug-induced acute interstitial nephritis. Given the temporal relationship between the initiation of furosemide in this patient and his worsening kidney function makes it the likely offending agent. He was observed off furosemide without any immunosuppressant treatment. The patient’s creatinine level gradually trended down and ultimately returned to his baseline at a one-month follow-up. Discussion Furosemide is a loop diuretic, often used in patients to prevent volume overload. Therefore, furosemide is often implicated as a cause of pre-renal acute kidney injury (AKI) secondary to volume depletion. However, interstitial inflammation as a mechanism of furosemide-induced kidney injury is uncommon and can often be overlooked as a potential cause, especially in patients with long medication lists. In such patients, a causal link can be established by correlating the onset of decline in kidney function with the time of initiation of a new drug and resolution of AKI after discontinuation of the drug.