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  • Fever.

  • Transient maculopapular rash.

  • Acute or chronic in nature.

  • Pyuria, white blood cell casts, and hematuria.


Acute interstitial nephritis accounts for 10–15% of cases of intrinsic renal failure. An interstitial inflammatory response with edema and possible tubular cell 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 as idiopathic conditions. The most common drugs implicated are penicillins and cephalosporins, immune checkpoint inhibitors, sulfonamides and sulfonamide-containing diuretics, NSAIDs, proton pump inhibitors, 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 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. The urine often contains white cells (95%), red cells, and white cell casts. Proteinuria is often present, particularly in NSAID-induced interstitial nephritis, but is usually modest (less than 2 g/24 h). Eosinophiluria is neither very sensitive nor specific for interstitial nephritis; evaluation for eosinophiluria is not advised. Although the clinical history and laboratory data often give clues to 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 all referred 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 removal of the inciting agent. If kidney injury persists, a short course of corticosteroids can be considered, although the data to support their use are not substantial, and their efficacy may depend on the elapsed time between onset of AKI and their initiation. Short-term, high-dose methylprednisolone (0.5–1 g/day intravenously for 1–4 days) or prednisone (60 mg/day orally for 1–2 weeks) followed by a prednisone taper can be used in more severe cases of drug-induced interstitial nephritis.

Moledina  DG  et al. Treatment of drug-induced acute tubulointerstitial nephritis: the search for better evidence. Clin J Am Soc Nephrol. 2018;13:1785.
[PubMed: 30397028]  
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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