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• W3142783272 abstract "To the Editor: Transplant patients are excluded from immunotherapy trials and therefore require more attention if such a treatment is deemed necessary. There should be an established procedure for managing immune-related adverse events (irAEs) secondary to PD-1/PD-L1 blockade because of the high rejection rate (37%1Fisher J, Zeitouni N, Fan W, Samie FH. Immune checkpoint inhibitor therapy in solid organ transplant recipients: a patient-centered systematic review. J Am Acad Dermatol. 2019. https://doi.org/10.1016/j.jaad.2019.07.005.Google Scholar–80%2Saberianfar S Nguyen LS Manouchehri A et al.Solid organ transplant rejection associated with immune-checkpoint inhibitors.Ann Oncol. 2020; 31: 543-544Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar,3d’Izarny-Gargas T Durrbach A Zaidan M. Efficacy and tolerance of immune checkpoint inhibitors in transplant patients with cancer: a systematic review.Am J Transplant. 2020; 20: 2457-2465Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar) and the subsequent mortality, especially in non-kidney recipients.3d’Izarny-Gargas T Durrbach A Zaidan M. Efficacy and tolerance of immune checkpoint inhibitors in transplant patients with cancer: a systematic review.Am J Transplant. 2020; 20: 2457-2465Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar,4Abdel-Wahab N Safa H Abudayyeh A et al.Checkpoint inhibitor therapy for cancer in solid organ transplantation recipients: an institutional experience and a systematic review of the literature.J Immunother Cancer. 2019; 7 (https://doi.org/10.1186/s40425-019-0585-1.)Google Scholar CTLA4 agonist has been identified as a nivolumab antidote for fulminant myocarditis in naïve patients but it may be insufficient in primed patients with a much stronger alloimmune response. We will describe a cytokine storm induced by cemiplimab (a PD-1 blocking antibody) in a renal transplant patient, to reinforce physicians’ awareness of this process and guide therapeutic choice in tailored medications based on a cytokine profile analysis. An 81-year-old man presented with fever, hypotension, abdominal pain, and acute kidney injury. He had a history of two kidney transplantations (the last one 7 years ago) and moderately differentiated, infiltrating keratinizing squamous cell carcinoma (SCC) of the skin on the forehead. SCC was diagnosed 4 years ago, considered to be non-resectable and successfully treated with a combination of paclitaxel plus cetuximab (anti-EGFR) and then radiation therapy. He relapsed 1 year ago and was successively treated with paclitaxel plus cetuximab, carboplatin plus cetuximab, and vinorelbine. His immunosuppressive regimen based on tacrolimus, mycophenolic acid, and steroids was reduced to a single steroid dose of 10 mg/d 4 months before exposure to cemiplimab. The decision to treat with cemiplimab was made in consultation with the oncodermatology and organ transplantation teams. Seven days after the first cemiplimab injection, patient was admitted with suspected septic shock secondary to pyelonephritis. Serum creatinine rapidly deteriorated from 50 µmol/L 3 days before to 460 µmol/L on admission. CT scan excluded vascular thrombosis but revealed massive graft infiltration (Figure 1A). Screening for infectious disease was negative. Despite steroid administration at 1 mg/kg/d, the patient rapidly required dialysis. Transplantectomy 7 days after admission revealed massive kidney necrosis (Figure 1B). Infiltrating lymphocytes could not be precisely analyzed because of the destruction of renal parenchyma (Figure 1C; Figure S1). Screening for anti-HLA antibodies was negative. Unfortunately, transplantectomy led to surgical complications with an occlusive syndrome, bleeding gastroduodenal ulcers, and the patient died 2 months later of peritonitis and refractory septic shock while on chronic hemodialysis, without any improvement of SCC. To specifically describe this acute rejection through a systemic presentation, we retrospectively performed blood quantification of seven cytokines: IL-6 and IL-8 increased massively at admission and decreased after transplantectomy. Soluble CD163 exhibited a fourfold increase at admission, suggesting high macrophage activation that may participate in IL-6 overproduction (Figure 1D). To our knowledge, this is the first evidence of IL-6, IL-8, and sCD163 elevation after a single dose of PD1 blockade in a transplant patient that mimics sepsis secondary to an infection. The chronology strongly suggests a pharmacological cause and excludes other diagnoses, although successful treatment of renal patients with cemiplimab has previously been reported5Tsung I, Worden FP, Fontana RJ. A pilot study of checkpoint inhibitors in solid organ transplant recipients with metastatic cutaneous squamous cell carcinoma. Oncologist. 2020. https://doi.org/10.1002/onco.13539.Google Scholar and small series suggest reasonable safety and efficacy of anti-PD1 in transplant patients.6Kumar V Shinagare AB Rennke HG et al.The safety and efficacy of checkpoint inhibitors in transplant recipients: a case series and systematic review of literature.Oncologist. 2020; 25: 505-514Crossref PubMed Scopus (67) Google Scholar Our findings should underscore the relevance of inflammatory cytokine measurement when irAEs are suspected. Effect magnitude and steroid refraction suggest that when possible anti-IL8 or anti-IL6 signaling (e.g., tocilizumab) should be discussed to prevent acute renal graft intolerance syndrome and subsequent morbidities, especially since safety and benefits have previously been established in the target population for other irAEs7Stroud CRG Hegde A Cherry C et al.Tocilizumab for the management of immune mediated adverse events secondary to PD-1 blockade.J Oncol Pharm Pract. 2019; 25: 551-557Crossref PubMed Scopus (171) Google Scholar or hemophagocytic syndrome.8Faguer S Del Bello A Abravanel F Nicolau-Travers ML Kamar N. Tocilizumab for hemophagocytic syndrome in a kidney transplant recipient with COVID-19.Ann Intern Med. 2020; 173: 501-503Crossref PubMed Scopus (18) Google Scholar The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation. Additional supporting information may be found online in the Supporting Information section. Download .jpg (.15 MB) Help with files Fig S1" @default.
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• W3142783272 title "Cytokine storm induced by a PD1 inhibitor in a renal transplant patient" @default.
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