Abstract: SA-PO1157
De Novo Atypical Hemolytic Uremic Syndrome Triggered by COVID-19 and Pneumocystis jirovecii in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Infectious Diseases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Gu, Siwen, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
- Zhuang, Jing, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
- Yalikun, Dilina, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
- Qu, Yue, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
- Aierken, Ailima, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
- Jiang, Hong, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China
Introduction
Posttransplant atypical hemolytic uremic syndrome (aHUS) is a devastating complication frequently leading to early allograft failure. We report a rare case of de novo aHUS triggered by concurrent COVID-19 and Pneumocystis jirovecii pneumonia (PCP). With targeted complement inhibition, active thrombotic microangiopathy (TMA) significantly resolved, rescuing graft function.
Case Description
A 28-year-old male, 3 years post-kidney transplant, presented with fever (39.1°C) and dyspnea. Evaluation confirmed COVID-19 and PCP via bronchoalveolar lavage sequencing. Despite targeted antimicrobials, his serum creatinine (SCr) rose from 2.63 to 7.02 mg/dL. Concurrently, platelets plummeted to 14×10^9/L, and lactate dehydrogenase peaked at 550 U/L. Allograft biopsy demonstrated acute TMA with swollen endothelial cells, capillary thrombosis, and widened subendothelial space. Soluble C5b-9 was markedly elevated at 475 ng/mL. TTP and STEC-HUS were excluded; complement genetics were negative. He was diagnosed with aHUS and treated with eculizumab, steroid pulses, and temporary hemodialysis. Platelets rapidly normalized, SCr improved, dialysis was discontinued, and sC5b-9 dropped to 248 ng/mL. A repeat biopsy 5 months later confirmed remarkable histological resolution of active TMA lesions.
Discussion
Severe opportunistic co-infections can trigger catastrophic terminal complement-mediated TMA in renal allografts, even without underlying genetic mutations. Serial biopsies provided invaluable proof of tissue-level TMA reversal following C5 blockade. Prompt recognition and targeted eculizumab therapy successfully rescued allograft function and abrogated dialysis dependence in this highly complex scenario.
Acknowledgment
We sincerely thank the Clinical Research Center of Kidney Disease of Xinjiang Uygur Autonomous Region for their invaluable technical support.
Figure 1. Dynamic kidney histopathological changes following complement inhibition in de novo aHUS.