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  • Fever.

  • Transient maculopapular rash.

  • Acute or chronic in nature.

  • Pyuria, WBC casts, and hematuria.


Acute interstitial nephritis accounts for 10–15% of cases of intrinsic AKI. An interstitial inflammatory response with edema and possible tubular damage is the typical pathologic finding. Cell-mediated immune reactions prevail over humoral responses. T lymphocytes can cause direct cytotoxicity or release lymphokines that recruit monocytes and inflammatory cells.

Although drugs account for over 70% of cases, acute interstitial nephritis also occurs in infectious diseases, autoimmune disorders, or idiopathically. The most common drugs implicated are penicillins and cephalosporins, immune checkpoint inhibitors, sulfonamides and sulfonamide-containing diuretics, NSAIDs, PPIs, rifampin, and allopurinol. Infectious causes include streptococcal infections, leptospirosis, cytomegalovirus, histoplasmosis, and Rocky Mountain spotted fever. SLE, Sjögren syndrome, sarcoidosis, and cryoglobulinemia can also cause interstitial nephritis, though they are more classically associated with glomerulonephritis.


Clinical features may include fever (more than 80% of cases), rash (25–50%), arthralgias, and peripheral blood eosinophilia (80%). The classic triad of fever, rash, and arthralgias is present in only 10–15% of cases. Urine microscopy often reveals white cells (70%), red cells (50%), and white cell casts (15%). Proteinuria is often present, particularly in NSAID-induced interstitial nephritis, but is usually modest (less than 2 g/24 hour). Evaluation for eosinophiluria is not advised as it is neither sensitive nor specific for interstitial nephritis. Although the clinical history and laboratory data often suggest the diagnosis, kidney biopsy is sometimes needed.


Acute interstitial nephritis often carries a good prognosis, with recovery occurring over weeks to months. Urgent dialytic therapy may be necessary in up to one-third of patients before resolution, but patients rarely progress to ESKD. Those with prolonged oliguria and advanced age have a worse prognosis. Treatment consists of supportive measures and prompt removal of the inciting agent. If kidney injury persists despite removal of the culprit drug, corticosteroids should be considered, although data to support their use are limited, and their efficacy is diminished if started more than 1–2 weeks after onset of AKI. Short-term, high-dose methylprednisolone (0.25–0.5 g/day intravenously for 1–4 days) or prednisone (60 mg/day orally for 4–6 weeks) followed by a prednisone taper can be used in severe cases of drug-induced interstitial nephritis.

Perazella  MA  et al. Immune checkpoint inhibitor nephrotoxicity: what do we know and what should we do? Kidney Int. 2020;97:62.
[PubMed: 31685311]  
Shingarev  R  et al. Kidney complications of immune checkpoint inhibitors: a review. Am J Kidney Dis. 2019;74:529.
[PubMed: 31303350]  

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