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.
- Latency varies by agent and previous sensitisation: antibiotics may cause a relatively abrupt syndrome, whereas proton-pump inhibitor-associated disease can be subtle and delayed.
- Urinalysis may show sterile pyuria, microscopic haematuria and modest proteinuria; white-cell casts can support the diagnosis but are neither sensitive nor specific, and urine eosinophils are unreliable.
- NSAID-associated AIN may differ by having less systemic hypersensitivity and more marked proteinuria, occasionally with a minimal-change-type nephrotic presentation.
- Stop the likely culprit promptly, document the suspected reaction and avoid casual rechallenge. Also stop unnecessary co-nephrotoxins and adjust medicines that accumulate in AKI.
- Kidney biopsy is the diagnostic reference when uncertainty matters, recovery is absent or immunosuppression is contemplated; corticosteroids are a nephrology-led risk–benefit decision, not an automatic response to pyuria.
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.
Substantial albuminuria, dysmorphic haematuria, red-cell casts, severe hypertension, low complement or pulmonary haemorrhage point away from isolated interstitial nephritis and demand an urgent glomerulonephritis work-up.
Creatinine continues to rise or fails to improve after trigger withdrawal, particularly with an uncertain multi-causal illness. This should prompt early renal discussion about biopsy, prognostic fibrosis and whether specialist treatment is justified.
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.
- 3. Exclude haemodynamic injury and obstruction, and seek glomerular, infectious or systemic clues that would make AIN an incomplete explanation.
- 4. Discuss early with nephrology when AKI is severe, worsening, atypical or likely to need biopsy or immunosuppression.