Abstract: TH-PO069
Mimicking Ulcerative Colitis Flare-Ups Induced by Azathioprine Causes AKI
Session Information
- AKI: Liver Disease, Nephrotoxicity, Novel Therapeutics
November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Yanai, Mitsuru, Sapporo Tokushukai Hospital, Sapporo, Japan
- Araki, Makoto, Sapporo Tokushukai Hospital, Sapporo, Japan
Introduction
Inflammatory bowel disease (IBD) is correlated with various renal ailments, including renal lithiasis, glomerulonephritis, renal amyloidosis, and drug-induced nephropathy. But no prior reports have documented drug-induced renal dysfunction with azathioprine (AZA) in IBD.
Case Description
A 61-year-old male was referred to our facility for ulcerative colitis flare-up. He had previously tried various medications, including 5-aminosalicylic acid (5ASA), AZA, and anti-TNFα antibody. Achieving remission with 30 mg prednisolone (PSL), he began novel anti-IL12/23 antibody treatment. Over 8 weeks, the PSL dose was gradually reduced without relapse. During the second dose of the anti-IL12/23 antibody, AZA at 25 mg/day replaced PSL. The next morning, the patient experienced chills, fatigue, and worsening diarrhea (over 10 times per day) shortly after the morning dose. Diarrhea persisted, the patient lost appetite, and became anuric. Subsequently, on the fourth day after anti-IL12/23 antibody administration, the patient was ambulance-transported to our hospital. Compared to values from four days prior, white blood cell count increased from 7500 to 9130/µL, C-reactive protein level rose from 0.32 to 41.37 mg/dL, and creatinine level escalated from 1.01 to 8.29 mg/dL. Considering possible infectious enteritis or worsening ulcerative colitis, the patient promptly received intravenous fluids, antibiotics, and 30 mg PSL. Hemodialysis was initiated. On the fourth day of hospitalization, a renal biopsy revealed massive cellular infiltration of the interstitium, leading to the diagnosis of acute interstitial nephritis due to azathioprine hypersensitivity syndrome. The PSL dose was quickly increased to 60 mg. Renal function gradually improved, and dialysis was completed in three sessions. After one month, creatinine levels returned to baseline, and steroid treatment ceased. Subsequently, the patient received a third dose of the anti-IL12/23 antibody without any adverse events.
Discussion
Azathioprine hypersensitivity syndrome is a systemic allergic reaction to immunosuppressive drugs, resulting in acute interstitial nephritis in the kidneys. Severe inflammatory reactions of heightened intensity mimic an exacerbation of the underlying disease or sepsis, frequently leading to delayed treatment. Timely diagnosis and prompt administration of steroids can influence the renal prognosis.