Abstract: FR-PO023

Using Steroids in Acute Interstitial Nephritis Secondary to Immune Checkpoint Inhibitors

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Verma, Sean, University of South Florida, Tampa, Florida, United States
  • Shirley, Kayla, University of South Florida, Tampa, Florida, United States
  • Bassil, Claude, University of South Florida, Tampa, Florida, United States

Immune checkpoint inhibitors (ICI), both anti programmed death ligand 1 (PD-L1) and anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) antibodies, are novel immunotherapies that have transformed the treatment of non-small cell lung cancer, renal cell cancer, and metastatic melanoma. Renal toxicities associated with ICI are a rare side effect that must be elucidated.


A 78 year old man with metastatic lung adenocarcinoma on PD-L1 antibody durvalumab and anti-CTLA-4 antibody tremelimumab had acute kidney injury (AKI) with creatinine of 3.2 mg/dL (baseline 1.4 mg/dL) on routine labs. He completed 4 cycles of therapy and his last cycle finished 1 month ago. Labs were notable for bicarbonate 12 meq/L and phosphorus 4.7 mg/dL. Urinalysis revealed pH 7, specific gravity 1.008, and hyaline casts. Urine eosinophils were positive and he was started on intravenous methylprednisolone at 1mg/kg BID (80 mg BID) for acute interstitial nephritis (AIN). With 4 days of methylprednisolone 80 mg BID, creatinine improved to 2.3 mg/dL. He was transitioned to 80 mg PO prednisone daily for 2 days with creatinine improving to 1.9 mg/dL. He was discharged on 60 mg prednisone daily with instructions to decrease prednisone by 10 mg every 5 days. One week later creatinine was 1.4 mg/dL and his creatinine continues to be at baseline 2 months later.


ICI upregulate the patient’s innate anti-tumor T cell response to the tumor and have been shown to significantly decrease tumor progression in comparison to standard treatment options previously available. Renal injury has seldomly been described in cases of both CTLA-4 and PD-L1 antibodies alone or in combination, though combination increases the risk of AKI. A variety of renal injury may occur, though AIN appears most reported. Hematuria, eosinophilia, worsening or new hypertension, and nephrotic syndrome have occurred in a few cases. The pathogenesis of AIN with ICI is unclear but it is thought to be due to uncontrolled increased T regulatory cell activity in which auto-reactive T cells infiltrate the kidney and cause cytotoxic injury. PD-L1 knockout mice have shown to spontaneously develop granulomatous AIN. Treatment is based on case reports and anecdotal data with prednisone 1 mg/kg over a taper of 1-2 months. A renal biopsy can be considered in cases with unclear etiology of AKI or if steroids aren’t effective.