[Thrombotic microangiopathy caused by vitamin B12 and folate deficiency (pseudo-TMA)]

Thrombotic microangiopathies (TMA) are characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage. As a rare but reversible cause, vitamin B12 and folate deficiency may present as thrombotic microangiopathy (pseudo-TMA) with hemolytic uremic syndrome (HUS)-like clinical features, posing a significant diagnostic challenge. A 56-year-old woman developed severe macrocytic anemia, thrombocytopenia, acute kidney injury, and laboratory signs of hemolysis. Investigations revealed marked folate deficiency, pronounced macrocytosis (MCV>120 fL), low haptoglobin levels, and markedly elevated lactate dehydrogenase. ADAMTS13 activity was reduced but not consistent with classical thrombotic thrombocytopenic purpura, while complement studies demonstrated secondary, consumptive activation. Infectious, autoimmune, malignant, and drug-related causes were excluded. The patient required transient continuous renal replacement therapy, plasma exchange, and corticosteroid treatment, followed by high-dose folate and vitamin B12 supplementation. After vitamin replacement, a rapid reticulocyte response, resolution of hemolysis, and complete hematologic remission were observed. This case highlights that folate and vitamin B12 deficiency can cause reversible pseudo-TMA with HUS-like presentation. Early recognition and targeted vitamin supplementation are essential, as they may prevent unnecessary invasive or costly therapies. Orv Hetil. 2026; 167(14): 556-559.