Management of Acute Tubulointerstitial Nephritis

Abstract

Acute tubulointerstitial nephritis (ATIN) is an important cause of acute kidney injury and acute kidney disease globally and is characterized by immune cell infiltration into the renal tubulointerstitium, causing inflammation, tubular injury, and ultimately fibrosis. Drug-induced hypersensitivity is the most common cause (>70%); however, infections and systemic autoimmune conditions are additional triggers, with a small percentage having idiopathic ATIN. Diagnosis requires a high index of suspicion as there can be significant clinical and laboratory overlaps between the various types of ATIN and other etiologies of acute kidney injury. Oligosymptomatic acute kidney injury with a lack of urinary findings is a common presentation, adding to the diagnostic challenge. Kidney biopsy is the gold standard for diagnosis. Management of ATIN focuses on promptly identifying and addressing the underlying trigger. Given that injury is primarily immune-mediated, immunosuppressive therapy has been explored extensively in the treatment of noninfectious ATIN; however, robust randomized controlled trials are lacking to guide specific treatments. With cessation of the immune trigger and prompt treatment initiation, ATIN generally has a favorable renal prognosis. However, delay in diagnosis or increased exposure to the culprit agent can result in irreversible interstitial fibrosis and CKD.