Synopsis
Recognise drug-related and systemic acute interstitial nephritis, withdraw the likely trigger, exclude mimics and involve nephrology early when diagnosis or immunosuppression is uncertain.
- Acute interstitial nephritis is an inflammatory tubulointerstitial cause of AKI, most often triggered by medicines but also associated with infection, immune disease and less common infiltrative disorders.
- Common medication groups include beta-lactam and other antibiotics, proton-pump inhibitors, NSAIDs and allopurinol; immune-checkpoint inhibitors create a specialist oncology–renal presentation.
- The classic triad of fever, rash and eosinophilia is uncommon. Its absence should not reassure when creatinine rises after a plausible exposure and urine findings suggest tubulointerstitial inflammation.
Key red flags
Fever, a new maculopapular eruption, eosinophilia, arthralgia or liver-test disturbance can support a systemic drug reaction. Assess mucosa, skin pain, blistering and organ involvement because severe cutaneous reactions require emergency specialist care.
Investigation priorities
Identify a plausible culprit and estimate latency, dose exposure, dechallenge and competing nephrotoxins.
Management branches
Unexplained AKI follows a plausible medicine or systemic inflammatory exposure.
- 1. Reconstruct every medicine and illness exposure with start, stop and administration dates, including over-the-counter analgesia and recent courses completed before admission.
- 2. Examine for rash, fever, arthralgia, lymphadenopathy, mucosal or hepatic involvement and measure urine findings, culture, albuminuria and renal trajectory.
Key medicines
Systemic corticosteroid for selected biopsy-supported or highly probable AINThe agent, route, weight-based or fixed regimen and taper are prescribed by nephrology under the current local protocol after infection and diagnostic uncertainty have been addressed.