ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO0102

Use of Azathioprine in Treating Severe Corticosteroid-Resistant Acute Interstitial Nephritis

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials


  • Lodhi, Sameed Khalid, Carle Foundation, Urbana, Illinois, United States
  • Jasti, Sravan, Carle Foundation, Urbana, Illinois, United States
  • Ghazanfar, Hareem, King Edward Medical University, Lahore, Pakistan

Acute interstitial nephritis (AIN) is a pattern of renal injury characterized by inflammatory infiltrate in renal interstitium leading to decline in renal function. It is commonly caused by drugs such as penicillin, diuretics and proton pump inhibitors. Other causes include autoimmune diseases or systemic infections. Treatment involves removing the offending agent and steroids in severe cases. We describe a case of drug induced severe AIN refractory to steroids that is treated with azathioprine, an immunosuppressant drug that inhibits purine synthesis.

Case Description

A 20 year old Caucasian female with past medical history of gastroesophageal reflux disease (GERD) presented to the emergency with severe nausea, vomiting and oliguria. She had been taking omeprazole for 2 weeks prior to presentation. Initial labs indicated eosinophilia, raised creatinine levels of 3.5 mg/dl and Blood Urea Nitrogen of 27 mg/dl. Renal biopsy was done which showed severe acute interstitial nephritis with raised eosinophils. The diagnosis of Acute Kidney Injury secondary to drug induced AIN was made and patient was given pulse dose steroids for 3 days. She was discharged on 60 mg of prednisolone daily. A month later, the patient’s creatinine improved to 1.75 from a peak of 6.27 mg/dl. The steroid dose was tapered to 40 mg. However, the creatinine raised to 2.7 mg/dl again due to which prednisolone dose was increased to 60 mg/dl. Kidney function did not improve even after 2 months and re-biopsy revealed ongoing interstitial nephritis. Consequently, the patient was given a trial of azathioprine 200 mg daily with reduced prednisolone dose (40 mg/dl). Creatinine levels decreased moderately after 2 weeks to 1.70 mg/dl due to which the prednisolone dose was further tapered to 20 mg/dl.


In past, azathioprine has shown promise in treatment of lupus nephritis and IgA nephropathy. To our knowledge, this is the first reported case of successful treatment of steroid resistant severe drug induced AIN with azathioprine. As it has lesser side effects and better compliance than steroids, it is suggested that azathioprine may be considered in future as an adjuvant or alternative first line of treatment for AIN. Larger, randomized clinical trials need to be conducted in order to establish optimal dosing and long term effectiveness of azathioprine in treating AIN.