Abstract: SA-PO0697
Serum Sickness Disease in Pediatric Transplant Patients
Session Information
- Pediatric Nephrology: Transplantation, Hypertension, AKI, Genetics, and Developmental Diseases
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pediatric Nephrology
- 1900 Pediatric Nephrology
Authors
- Boakye, Anita Amma Akomaa, Indiana University School of Medicine, Indianapolis, Indiana, United States
- Nailescu, Corina, Indiana University School of Medicine, Indianapolis, Indiana, United States
- Pottanat, Neha D., Indiana University School of Medicine, Indianapolis, Indiana, United States
Introduction
Rabbit-derived anti-thymocyte globulin (ATG), used for induction immunosuppression and rejection treatment in kidney transplants, can cause serum sickness disease (SSD) in 7-27% of kidney transplant patients. Symptoms often mimic infection, delaying diagnosis and increasing morbidity. We present two patients who experienced SSD after exposure to ATG within the same week.
Case Description
Patient one is a 16-year-old female who underwent kidney transplantation with induction using rabbit-derived ATG (no previous exposure to ATG). She presented 13 days post-ATG exposure with right hip pain, and diffuse arthralgia. Labs showed high inflammatory markers (WBC 16.4k, ESR 96, CRP 207), low complements (C3 75, C4 <8), and AKI (Cr 3.23, prior 0.75), and pyuria with negative urine and blood culture. She was treated empirically for SSD with high-dose methylprednisolone followed by a rheumatology directed prednisone taper. SSD was confirmed with positive anti-rabbit antibodies. Kidney biopsy obtained due to persistently elevated serum creatinine showed pathology consistent with acute cellular rejection, treated with alemtuzumab.
Patient two is a 15-year-old female who was treated for acute cellular rejection with ATG (previous history of exposure to ATG). She presented to the ED 15 days post-ATG exposure with low grade fever, neck and shoulder arthralgia, and a left knee effusion. Labs showed elevated inflammatory markers (WBC 16.6k, ESR 120, CRP 28), low-normal C4 (14), and AKI (Cr 1.57, baseline 1.15). She was treated empirically for SSD with high-dose methylprednisolone—positive anti-rabbit antibodies confirmed the diagnosis. Elevated serum creatinine improved to baseline with treatment of SSD. Both patients denied previous contact with rabbits.
Discussion
SSD presents a diagnostic challenge to patients with kidney transplants. Aside from its immunologic etiology, it increases the risk of infection and acute kidney injury, increasing the risk of graft loss. While rabbit-derived ATG is effective for T-cell depletion, development of anti-rabbit antibodies can limit effectiveness, as shown in patient one, who required re-induction immunosuppression with alemtuzumab. Recognizing the common symptoms of SSD after ATG exposure helps aid in timely identification and prevention of graft loss. We also describe an effective treatment pathway for SSD due to ATG not previously described in literature.