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Background <p>Renal allograft artery thrombosis (RAAT) is a severe vascular complication that typically occurs within the first month after transplantation and frequently results in graft loss. Although most cases are attributed to surgical or technical factors, we report a rare case of late-onset RAAT secondary to acute antibody-mediated rejection (ABMR), further complicated by severe drug-induced neutropenia.</p> Case presentation <p>A 32-year-old female with end-stage renal disease underwent an ABO-compatible living-donor kidney transplantation, with an uneventful early postoperative course. On postoperative day (POD) 83, she presented with acute oliguria. Doppler ultrasonography revealed absent allograft arterial flow, confirming RAAT. Emergent thrombolysis restored macrovascular patency; however, renal function failed to recover, necessitating a return to hemodialysis. During readmission for peritoneal dialysis (PD) catheter placement, she developed life-threatening neutropenia, attributed to drug-induced myelosuppression, predominantly from mycophenolate mofetil with possible additive effects of ganciclovir and trimethoprim-sulfamethoxazole. Concurrently, markedly elevated donor-derived cell-free DNA (dd-cfDNA) levels (plasma 1.36%, urine 11.43%) suggested active rejection. Given the unsalvageable graft and severe neutropenia, allograft nephrectomy with PD catheter placement was performed. Histopathology confirmed acute ABMR with diffuse C4d positivity. Immunosuppression was discontinued, and leukocyte counts normalized postoperatively.</p> Conclusions <p>This case illustrates that late-onset RAAT can serve as a catastrophic complication of acute ABMR. Furthermore, it highlights the clinical utility of dd-cfDNA as a non-invasive diagnostic adjunct when biopsy is contraindicated, and underscores the complex management dilemmas arising from concurrent graft failure and severe drug toxicity, which ultimately necessitate a multidisciplinary, patient-centered approach.</p>

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Transplant renal artery thrombosis caused by acute rejection : a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月1日

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  • Junyan Fang,
  • Ruolin Li,
  • Yingxin Xie,
  • Shaojun Liu,
  • Yingli Liu

摘要

Background

Renal allograft artery thrombosis (RAAT) is a severe vascular complication that typically occurs within the first month after transplantation and frequently results in graft loss. Although most cases are attributed to surgical or technical factors, we report a rare case of late-onset RAAT secondary to acute antibody-mediated rejection (ABMR), further complicated by severe drug-induced neutropenia.

Case presentation

A 32-year-old female with end-stage renal disease underwent an ABO-compatible living-donor kidney transplantation, with an uneventful early postoperative course. On postoperative day (POD) 83, she presented with acute oliguria. Doppler ultrasonography revealed absent allograft arterial flow, confirming RAAT. Emergent thrombolysis restored macrovascular patency; however, renal function failed to recover, necessitating a return to hemodialysis. During readmission for peritoneal dialysis (PD) catheter placement, she developed life-threatening neutropenia, attributed to drug-induced myelosuppression, predominantly from mycophenolate mofetil with possible additive effects of ganciclovir and trimethoprim-sulfamethoxazole. Concurrently, markedly elevated donor-derived cell-free DNA (dd-cfDNA) levels (plasma 1.36%, urine 11.43%) suggested active rejection. Given the unsalvageable graft and severe neutropenia, allograft nephrectomy with PD catheter placement was performed. Histopathology confirmed acute ABMR with diffuse C4d positivity. Immunosuppression was discontinued, and leukocyte counts normalized postoperatively.

Conclusions

This case illustrates that late-onset RAAT can serve as a catastrophic complication of acute ABMR. Furthermore, it highlights the clinical utility of dd-cfDNA as a non-invasive diagnostic adjunct when biopsy is contraindicated, and underscores the complex management dilemmas arising from concurrent graft failure and severe drug toxicity, which ultimately necessitate a multidisciplinary, patient-centered approach.