De novo thrombotic microangiopathy after kidney transplantation

De novo thrombotic microangiopathy (TMA) after kidney transplantation is a serious condition that develops in patients who have received a kidney transplant but had no prior history of TMA before transplantation. It is classified under thrombotic microangiopathies (ICD-10: M31.1) and is characterized by damage to the small blood vessels (microangiopathy) of the transplanted kidney, leading to formation of blood clots in the microvasculature. This condition primarily affects the renal graft but can also have systemic manifestations. Key clinical features include microangiopathic hemolytic anemia (destruction of red blood cells as they pass through damaged small vessels), thrombocytopenia (low platelet count), and progressive renal graft dysfunction that may lead to graft loss if untreated. The condition can be triggered by multiple factors related to the transplant setting, including calcineurin inhibitor toxicity (cyclosporine or tacrolimus), viral infections (such as cytomegalovirus or BK virus), antibody-mediated rejection, and ischemia-reperfusion injury. In some cases, complement dysregulation plays a role, particularly involving mutations or autoantibodies affecting the alternative complement pathway. Patients may present with rising serum creatinine, decreased urine output, hypertension, and laboratory findings consistent with hemolysis such as elevated lactate dehydrogenase, low haptoglobin, and schistocytes on peripheral blood smear. Treatment depends on the underlying cause and may include modification or withdrawal of calcineurin inhibitors, switching to mTOR inhibitors or other immunosuppressive regimens, plasma exchange or plasmapheresis, and in complement-mediated cases, treatment with the complement C5 inhibitor eculizumab. Early recognition and intervention are critical to preserving graft function. Despite treatment, de novo post-transplant TMA carries a significant risk of graft loss and patient morbidity.

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