Neonatal atypical hemolytic uremic syndrome is characterized by hemolytic anemia, thrombocytopenia and thrombotic microangiopathy. Disease caused by a genetic disorder in the alternative complement pathway. Although the traditional treatment methods are plasma infusion and plasmapheresis, C5 complement inhibitor eculizumab is the first treatment option in recent years. Here, we present 5 days old male newborn with direct/indirect hyperbilirubinemia, anemia, thrombocytopenia, hypertension and oliguria. Despite intensive phototherapy hiperbilirubinemia persisted and exchange transfusion was done. After exchange transfusion, his symptoms decreased gradually in 2 days. Two weeks after exchange transfusion, anemia, thrombocytopenia and oliguria occurred again. Hemodiafiltration was started. In genetic analysis, de novo homozygous factor H mutation (c.3493+1G>A) was revealed. Our patient is presented because of its rare occurrence in neonatal period and partly treated with blood exchange.
Oguz Han Kalkanli, Erkin Serdaroglu, Yesim Oymak, Ayca Aykut, Senem Alkan Ozdemir, Sebnem Calkavur and Tulin Gokmen Yildirim