Kidney allograft loss from intravascular thrombosis without cellular infiltration five days after transplant may indicate which primary rejection mechanism?

Kidney allograft loss from intravascular thrombosis without cellular infiltration five days after transplant may indicate which primary rejection mechanism?

• A. Hyperacute rejection
• B. Accelerated humoral rejection
• C. Acute humoral rejection
• D. Acute cellular rejection

Answer: (B)

Timing and pattern of vascular injury help distinguish rejection types. Intravascular thrombosis of graft vessels with little or no cellular infiltration occurring around five days after transplant points to an antibody-driven process rather than T-cell–mediated damage. This is the hallmark of accelerated humoral rejection: preformed or rapidly formed donor-specific antibodies target graft endothelium, activate complement, and provoke swift vascular injury with thrombosis. Because the injury is antibody- and complement–mediated, the typical lymphocytic infiltrate seen in cellular rejection is minimal. Hyperacute rejection would happen within minutes to hours with widespread thrombosis right away; acute humoral rejection can occur over days to weeks but often shows more pronounced evidence of antibody activity and vascular injury, and acute cellular rejection features prominent T-cell–driven interstitial infiltration and endothelitis. Thus, the described scenario best fits accelerated humoral rejection.

Timing and pattern of vascular injury help distinguish rejection types. Intravascular thrombosis of graft vessels with little or no cellular infiltration occurring around five days after transplant points to an antibody-driven process rather than T-cell–mediated damage. This is the hallmark of accelerated humoral rejection: preformed or rapidly formed donor-specific antibodies target graft endothelium, activate complement, and provoke swift vascular injury with thrombosis. Because the injury is antibody- and complement–mediated, the typical lymphocytic infiltrate seen in cellular rejection is minimal. Hyperacute rejection would happen within minutes to hours with widespread thrombosis right away; acute humoral rejection can occur over days to weeks but often shows more pronounced evidence of antibody activity and vascular injury, and acute cellular rejection features prominent T-cell–driven interstitial infiltration and endothelitis. Thus, the described scenario best fits accelerated humoral rejection.