Abstract: FR-PO024
Acute Tubulointerstitial Nephritis Induced by Anti-PD-1 Antibody: An Analysis of Infiltrating Cells in the Kidney
Session Information
- Fellows/Residents Case Reports: AKI and Drug-Related Interactions
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Tabei, Akifumi, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Ikeuchi, Hidekazu, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Nakasatomi, Masao, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Sakairi, Toru, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Kaneko, Yoriaki, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Maeshima, Akito, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Nojima, Yoshihisa, Japan Red Cross Maebashi Hospital, Maebashi, Gunma, Japan
- Hiromura, Keiju, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
Background
Nivolumab, an anti-PD-1 antibody, is one of the immune checkpoint inhibitors (ICIs), which are increasingly used as anti-cancer agents. It has been known to induce various autoimmune diseases in some patients, such as thyroiditis, pneumonitis and pancreatitis, via disruption of immune tolerance. As for kidneys, acute interstitial nephritis has recently been reported. However, the precise renal pathology has not been well understood yet.
Methods
A 57-year-old man was admitted to our department due to an acute increase of serum creatinine (SCr). He had been treated with nivolumab for stage IV lung cancer for 2 months with 2 weeks interval. On the 5th scheduled administration day, he was found to have an elevated SCr level from 0.80 mg/dL to 1.57 mg/dL. Nivolumab was stopped and he was referred to our department and admitted 8 days later. Renal biopsy was performed immediately. A marked infiltration of inflammatory and immune cells was observed in tubulointerstitial area. Immunohistochemical staining revealed that infiltrating cells were positive for CD3 (T cell), CD20 (B cell), CD68 (macrophage), CD163 (M2 macrophage), BDCA-1 (dendritic cell) and DC-SIGN (dendritic cell). Among these cells, CD68 and CD163 were predominant, followed by CD3. Proton pump inhibitor (PPI), rabeprazole, was discontinued, because previous reports showed a possible association between PPI and tubulointerstitial nephritis under the treatment of ICIs. By the treatment with 50 mg/day of prednisolone, the peaked SCr of 3.48 mg/dL retuned to baseline level within 2 months.
Conclusion
Just recently, several reports showed increased T cells accumulation in ICIs-induced acute tubulointerstitial nephritis. Our case highlights a potential role of macrophage, as well as T cells, in the pathogenesis of interstitial nephritis caused by anti-PD-1 antibody.