Acute interstitial nephritis (AIN) is an immune-mediated inflammatory condition affecting the renal interstitium and tubules, representing approximately 15-27% of all cases of acute kidney injury (AKI) requiring biopsy. The hallmark of AIN is inflammatory cell infiltration of the renal interstitium with tubular damage in the absence of primary glomerular or vascular pathology. The most common cause is drug hypersensitivity (accounting for 70-75% of cases), followed by autoimmune conditions (10-15%) and infections (5-10%). The registered nurse plays a critical role in identifying the offending agent, monitoring renal function trends, and managing the supportive care required during the recovery period. Drug-induced AIN is a type IV (delayed-type) hypersensitivity reaction mediated by T-lymphocytes rather than antibodies. When a drug or its metabolite acts as a hapten (a small molecule that alone cannot trigger an immune response), it binds to renal tubular proteins, forming a hapten-carrier complex that is processed and presented by antigen-presenting cells (dendritic cells, macrophages) to T-helper lymphocytes via MHC class II molecules. The activated T-cells release pro-inflammatory cytokines (interferon-gamma, interleukin-2, tumor necrosis factor-alpha) that recruit additional inflammatory cells -- cytotoxic...