International Journal of Advances in Nephrology Research

Thrombotic microangiopathy (TMA) is one of the most severe complications consequent to kidney transplant that predominantly affects the renal microvasculature. It is a histological characteristic of antibody-mediated rejection (AMR) and can lead to graft failure, especially in highly sensitized, cross-match positive kidney transplant recipients. The clinical features of TMA include platelet thrombi and aggregation, thrombocytopenia, microangiopathic hemolytic anemia, and tissue ischemia with organ failure. The underlying mechanism is usually a sequalae of combined acute coagulopathy and complement activation. In kidney transplant patients, de novo TMA can develop without a prior history or recurrent TMA as a continuation of disease in the native kidney. Both types are associated with poor graft prognosis and patient outcomes post-transplant. Overall, TMA can lead to graft failure in up to 50% of cases with a significant risk of mortality. Genetic testing, early diagnosis and treatment, as well as a thorough understanding of pathogenic pathways are crucial for its management. The treatment approach usually targets the causative factor, but some forms may require more aggressive or combined interventions. Plasma exchange and complement blockade with eculizumab are among the currently available therapies. Eculizumab is effective for both de novo and recurrent TMA post-transplant. But there is still a need to optimize the patient profile and duration of this therapy for its maximum benefits, along with exploring new alternate therapeutics. This review gives an overview of the types of TMA post-kidney transplant along with their pathophysiology, risk factors, incidence, and available treatment options.