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Kidney Week

Abstract: FR-PO0465

Steroid-Dependent Acute Interstitial Nephritis Treated with Infliximab: A Case Report

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Sandhu, Sharneet K., Massachusetts General Hospital, Boston, Massachusetts, United States
  • Al Jurdi, Ayman, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Seethapathy, Harish Shanthanu, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Efe, Orhan, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Wang, Qiyu, Brigham and Women's Hospital, Boston, Massachusetts, United States
Introduction

Glucocorticoids are the first-line treatment for acute interstitial nephritis (AIN). However, some patients may experience disease relapse with steroid taper and become steroid-dependent, and the etiologies can remain unclear. Tumor necrosis factor-α (TNF-α) blockade with infliximab has been used in checkpoint inhibitor-associated AIN as a steroid-sparing strategy, but its role in other causes of AIN is not well defined. We report a case with severe persistent AIN of unclear etiology that failed steroid taper and mycophenolate mofetil (MMF) and was successfully treated with infliximab.

Case Description

A 62-year-old man presented with fevers, night sweats, and acute kidney injury. CT suggested pyelonephritis versus an infiltrative process, with negative infectious workup. PPIs and NSAIDs were discontinued. Further workup showed elevated inflammatory markers and negative or normal autoimmune serologies. Kidney biopsy showed severe neutrophil-predominant AIN with tubulitis, negative immunofluorescence staining, and <10% interstitial fibrosis. High-dose prednisone led to initial partial improvement of creatinine, but it relapsed quickly during prednisone taper. MMF was started as a steroid-sparing agent without effect. He had a second relapse while being tapered off prednisone. At this time, he received IV methylprednisolone with recycling of prednisone taper, and he received 1 dose of infliximab with partial improvement in creatinine. A repeat biopsy at 6 months showed chronic active interstitial nephritis with a lymphocyte-predominant infiltrate, and marked progression in interstitial fibrosis (40%). Given steroid-dependent, progressive AIN, infliximab was reinitiated with monthly maintenance, allowing discontinuation of prednisone with stable kidney function (Figure 1).

Discussion

This report illustrates a favorable response and steroid-sparing effect of infliximab in a case of steroid-dependent AIN of unclear etiology, and suggests TNF-α inhibition may be a treatment option in selected cases of refractory AIN.