A case of overcoming De Novo thrombotic microangiopathy associated with hyperacute rejection in a living donor ABO-incompatible kidney transplantation despite severe intraoperative graft injury.

A 19-year-old male with end-stage renal disease caused by vesicoureteral reflux, hypertension, and type 2 diabetes mellitus underwent preemptive kidney transplantation using his mother's left kidney. This was an ABO-incompatible kidney transplant between a recipient with blood type O and a donor with blood type B. Therefore, plasma exchange and rituximab administration were performed preoperatively as desensitization therapy. Immediately after vascular anastomosis, blood flow in the transplanted renal cortex was assessed using ultrasonography, which was deemed adequate. Nonetheless, the urine output did not increase. Ultrasound re-evaluation revealed an elevated vascular resistance index in the transplanted renal cortex, raising hyperacute rejection suspicion. Rejection therapy was initiated before vesicoureteral anastomosis. Because concomitant de novo thrombotic microangiopathy (dnTMA) was also suspected, anticoagulant therapy was initiated. By the end of the surgery, the velocity of the renal cortical blood flow had decreased, prompting immediate plasma exchange. Hemodialysis was performed on postoperative day (POD) 0 but was not required thereafter. Serum creatinine levels remained at around 5-6 mg/dL for some time; nevertheless, they began to decrease on POD15, finally improving to 1.36 mg/dL on POD 65. A renal biopsy performed 1 h after reperfusion revealed fibrin thrombi and inflammatory cell infiltrates in the glomerular capillaries (g1), resulting in the diagnosis of dnTMA due to hyperacute rejection. The cause of hyperacute rejection was possibly HLA-DP donor-specific antibody. This report describes a case in which the prompt treatment for dnTMA due to hyperacute rejection preserved graft function.