Cytokine Release Syndrome Following Thymoglobulin Induction in a Kidney Transplant Recipient with Lupus Nephritis: A Case Report

Introduction: Cytokine release syndrome (CRS) is a rare but potentially life-threatening complication of antithymocyte globulin (ATG) therapy. Although well described in hematologic malignancies and immunotherapy, CRS remains underrecognized in solid organ transplantation. We present a case of CRS following ATG induction in a young woman with lupus nephritis undergoing deceased donor kidney transplantation. Case Description: A 22-year-old female with end-stage kidney disease from class IV lupus nephritis underwent deceased-donor kidney transplantation. Induction included rabbit-derived Thymoglobulin (1.5 mg/kg), methylprednisolone, and diphenhydramine. Following successful transplantation and extubation, she developed acute respiratory distress, fever (38.1 C), hypoxia (< 92%), hypotension (78/35 mmHg), and tachycardia (HR 112 bpm). Initial treatment with IV epinephrine and diphenhydramine failed to improve symptoms. The patient was reintubated for respiratory failure, requiring vasopressors and mechanical ventilation support. Bedside echocardiography showed biventricular dilation with an ejection fraction <15%. Labs revealed lactic acidosis (25.1 mmol/L), leukocytosis (21.1 x103/μL), IL-6 (1,047 pg/mL), CRP (11.2 mg/dL), and ferritin >15,000 ng/mL. Infectious workup, including cultures and imaging, was negative. The diagnosis of grade 4 CRS was established based on fever, hypotension requiring multiple vasopressors, and intubation. She was placed on veno-arterial ECMO, dobutamine, and continuous renal replacement therapy (CRRT) for delayed graft function. Treatment included a single dose of tocilizumab (IL-6 receptor blocker) and two doses of basiliximab for the kidney transplant. Eventually, the patient’s condition improved, with inflmatory markers trending downwards, and kidney function improving, prompting decannulation of ECMO and cessation of renal replacement therapy. She was discharged home with stable graft function, with Cratinine 1.2 mg/dL Discussion: This case helps illustrate the importance of recognizing CRS as a potential differential diagnosis in transplant recipient patients who present with systemic inflammatory response after ATG. CRS can be mistaken for acute rejection, but early recognition and prompt management, favor better outcomes.

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Publication Details

Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025ncn0pssh
Primary Topic
Renal Transplantation Outcomes and Treatments
Type
article
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article

Cytokine Release Syndrome Following Thymoglobulin Induction in a Kidney Transplant Recipient with Lupus Nephritis: A Case Report

Journal of the American Society of Nephrology
Renal Transplantation Outcomes and Treatments
article

Cytokine Release Syndrome Following Thymoglobulin Induction in a Kidney Transplant Recipient with Lupus Nephritis: A Case Report

article en

Abstract

Introduction: Cytokine release syndrome (CRS) is a rare but potentially life-threatening complication of antithymocyte globulin (ATG) therapy. Although well described in hematologic malignancies and immunotherapy, CRS remains underrecognized in solid organ transplantation. We present a case of CRS following ATG induction in a young woman with lupus nephritis undergoing deceased donor kidney transplantation. Case Description: A 22-year-old female with end-stage kidney disease from class IV lupus nephritis underwent deceased-donor kidney transplantation. Induction included rabbit-derived Thymoglobulin (1.5 mg/kg), methylprednisolone, and diphenhydramine. Following successful transplantation and extubation, she developed acute respiratory distress, fever (38.1 C), hypoxia (< 92%), hypotension (78/35 mmHg), and tachycardia (HR 112 bpm). Initial treatment with IV epinephrine and diphenhydramine failed to improve symptoms. The patient was reintubated for respiratory failure, requiring vasopressors and mechanical ventilation support. Bedside echocardiography showed biventricular dilation with an ejection fraction <15%. Labs revealed lactic acidosis (25.1 mmol/L), leukocytosis (21.1 x103/μL), IL-6 (1,047 pg/mL), CRP (11.2 mg/dL), and ferritin >15,000 ng/mL. Infectious workup, including cultures and imaging, was negative. The diagnosis of grade 4 CRS was established based on fever, hypotension requiring multiple vasopressors, and intubation. She was placed on veno-arterial ECMO, dobutamine, and continuous renal replacement therapy (CRRT) for delayed graft function. Treatment included a single dose of tocilizumab (IL-6 receptor blocker) and two doses of basiliximab for the kidney transplant. Eventually, the patient’s condition improved, with inflmatory markers trending downwards, and kidney function improving, prompting decannulation of ECMO and cessation of renal replacement therapy. She was discharged home with stable graft function, with Cratinine 1.2 mg/dL Discussion: This case helps illustrate the importance of recognizing CRS as a potential differential diagnosis in transplant recipient patients who present with systemic inflammatory response after ATG. CRS can be mistaken for acute rejection, but early recognition and prompt management, favor better outcomes.

Journal of the American Society of NephrologyVol. 36(10S)
Tulane University (US)
Good health and well-being
Openalex Percentile: Top 30%
Renal Transplantation Outcomes and Treatments
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