Cytomegalovirus viremia associated with systemic thrombotic microangiopathy after kidney transplantation: a case report.

BACKGROUND: Post-transplant thrombotic microangiopathy (PT-TMA) is an uncommon but severe complication of kidney transplantation associated with graft dysfunction and poor outcomes. Although infections have been recognized as potential triggers, systemic thrombotic microangiopathy associated with cytomegalovirus (CMV) infection remains rarely reported. Experimental and clinical evidence suggests that CMV may promote endothelial injury and complement activation, mechanisms that could contribute to the development of microangiopathic processes in transplant recipients. CASE PRESENTATION: We report the case of a 78-year-old kidney transplant recipient who developed de novo systemic thrombotic microangiopathy associated with CMV infection. The patient presented with thrombocytopenia, microangiopathic hemolytic anemia, and progressive graft dysfunction. Drug-induced TMA related to recent tacrolimus initiation was initially suspected; however, hematologic abnormalities persisted despite calcineurin inhibitor withdrawal. Further evaluation revealed significant CMV viremia (54,000 copies/mL), while additional viral, gastrointestinal infectious, and autoimmune evaluations did not identify a more likely alternative explanation. Intravenous ganciclovir therapy was initiated and later transitioned to oral valganciclovir. Following comprehensive management, including withdrawal of tacrolimus and targeted antiviral therapy, hemolysis resolved, platelet counts normalized, CMV viral load progressively declined until clearance, and renal graft function improved. Immunosuppression was subsequently reintroduced using a calcineurin inhibitor-free regimen with belatacept. CONCLUSION: CMV infection should be considered a plausible trigger of de novo post-transplant thrombotic microangiopathy, particularly in patients with persistent disease despite withdrawal of calcineurin inhibitors. Although post-transplant TMA is frequently multifactorial, early recognition of CMV viremia and timely comprehensive management addressing all contributing factors may be associated with favorable hematologic recovery and improvement of graft function.