Acute Drug-Induced Tubulointerstitial Nephritis: Current Perspectives on Diagnosis and Treatment

Abstract

Acute tubulointerstitial nephritis (ATIN) is one of the leading causes of acute kidney injury (AKI), accounting for approximately 15-27% of biopsy-proven cases of AKI. While some patients recover kidney function with timely intervention, a subset of patients may progress to chronic kidney disease and around one-third of the patients will require chronic dialysis. Drug-induced ATIN is the most common form and is often associated with nonsteroidal anti-inflammatory drugs, antibiotics, and proton pump inhibitors. Infections, autoimmune disorders, such as Sjögren's syndrome and sarcoidosis contribute to a smaller proportion of cases. Clinically, ATIN presents with a wide spectrum of symptoms ranging from asymptomatic AKI to systemic manifestations such as fever, rash, arthralgia, and eosinophilia. Urinalysis often reveals sterile pyuria, hematuria, and occasionally, white blood cell casts. Proteinuria is typically mild (<1.5 g/24 hours. Definitive diagnosis requires kidney biopsy, which reveals the presence of an extensive interstitial infiltrate, mainly composed of lymphocytes and monocytes, along with interstitial edema, and varying degrees of tubular injury. Early identification and management are critical to prevent irreversible kidney damage. So far, the optimal treatment of this entity is not yet well characterized but treatment strategies for ATIN must focus on prompt discontinuing the offending agent, supportive care, and corticosteroid therapy.