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Topic Note

Acute Interstitial Nephritis: MRCP Part 2 Notes

An immune-mediated cause of acute kidney injury — usually drug-induced — with eosinophilia, sterile pyuria and white cell casts.

MRCP Part 2Nephrology5 min read

Definition

Acute interstitial nephritis (AIN) is an immune-mediated inflammation of the renal interstitium and tubules that produces acute kidney injury. It is an important and often reversible cause of AKI, and a recurring MRCP theme because the culprit is usually a drug.

Pathophysiology

AIN is a hypersensitivity (typically T-cell mediated) reaction rather than a direct toxic effect, which is why it is idiosyncratic and not dose-related. The interstitium becomes oedematous and infiltrated with inflammatory cells, including eosinophils. Causes include:

  • Drugs (the majority): antibiotics (penicillins, cephalosporins, rifampicin, ciprofloxacin), NSAIDs, proton pump inhibitors, allopurinol, diuretics
  • Infections: e.g. staphylococci, streptococci, leptospirosis
  • Systemic/autoimmune disease: sarcoidosis, Sjögren syndrome, SLE

Clinical presentation

  • Acute kidney injury, often noticed as a rising creatinine days to weeks after starting a drug
  • The classic triad of fever, rash and arthralgia occurs in only a minority — its absence does not exclude AIN
  • Malaise; occasionally loin discomfort

Investigations

  • Rising creatinine; peripheral eosinophilia may be seen
  • Urinalysis: sterile pyuria, white cell casts, mild proteinuria, and sometimes eosinophiluria (low sensitivity and specificity)
  • Renal biopsy is the gold standard — interstitial oedema with an inflammatory infiltrate rich in eosinophils

Management

  • Stop the offending drug — the single most important step
  • Corticosteroids are commonly given to speed recovery, especially if function fails to improve after drug withdrawal (evidence is limited)
  • Supportive care and avoidance of further nephrotoxins

MRCP-specific traps

  • NSAID-induced AIN frequently occurs without the fever–rash–arthralgia triad and may be accompanied by nephrotic-range proteinuria (a combined minimal-change/interstitial picture).
  • AIN gives white cell casts; contrast this with the muddy-brown granular casts of acute tubular necrosis.
  • Because the reaction is idiosyncratic, it can occur even at standard therapeutic doses and after prolonged, previously tolerated use (classically with PPIs).

Summary

Acute interstitial nephritis is an immune-mediated, usually drug-induced cause of AKI. Look for sterile pyuria, white cell casts and eosinophilia. Stop the culprit drug promptly; steroids are often added. Recovery is common with early recognition.

nephrologyacute kidney injurydrug reactionsmrcp part 2

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