A 62-year-old male patient was admitted for close monitoring of anemia (hemoglobin level, 8.2 g/dl). Hemolytic anemia was observed; however, the direct antiglobulin test (DAT) result (standard tube method) was negative. Nevertheless, autoimmune hemolytic anemia (AIHA) was still suspected; therefore, a DAT (Colum method) and quantifying levels of red-blood-cell bound immunoglobulin G were performed, resulting in a definite diagnosis of warm AIHA. The patient also had an acute kidney injury (AKI) from the time of admission, which was poorly improved by supplemental fluids therapy alone. Therefore, renal biopsy was performed. Renal biopsy revealed acute tubular injury due to hemoglobin columns, and a diagnosed AKI caused by hemolysis due to AIHA. Following the definitive diagnosis of AIHA, the patient was treated with prednisolone, and after approximately 2 weeks, the anemia and nephropathy completely improved, which is maintained to this day. We report this case as a rare case of AKI induced by hemolysis of AIHA and a successful case of renal salvage by early administration of steroid.
Autoimmune hemolytic anemia is a disorder that is characterized by the destruction of red blood cells through an autoimmune process, such as temperature-dependent antibodies. The two predominant types, cold agglutinin and warm agglutinin disease, typically possess different underlying etiologies. Prompt recognition and workup of autoimmune hemolytic anemia should be prioritized to potentially uncover any underlying primary cause, such as malignancy.
Evans syndrome (ES) is a rare syndrome characterised by the association of autoimmune idiopathic hemolytic anemia (AIHA) with immune thrombocytopenia (ITP) and, less commonly, autoimmune neutropenia (AIN). ES may be primary or secondary to some aetiology, including, exceptionally, tuberculosis. We describe a case of association between pulmonary and medullary tuberculosis and Evans syndrome with an effective response to antitubercular treatment and corticosteroids.
Background: Thrombotic microangiopathy (TMA) is a rare, life-threatening disorder characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ damage. Atypical hemolytic uremic syndrome (aHUS) is even less common, comprising less than 10% of hemolytic uremic syndrome (HUS) cases. aHUS in postpartum is associated with poor maternal outcomes, with the majority of cases resulting in end-stage renal disease.
Mutations in the recombination-activating gene 1, a pivotal component essential for V(D)J recombination and the formation of T- and B-cell receptors, can result in autoimmune hemolytic anemia, a rare hematological condition characterized by the autoantibody-mediated destruction of red blood cells. Herein, we report the case of a 1-year-and-4-month-old girl who presented with progressively aggravated anemia, fever, and cough. Autoimmune hemolytic anemia was confirmed by bone marrow aspiration and Coombs test.
Background: Angiosarcoma is a rapidly proliferating vascular tumor that originates in endothelial cells of vessels. Rarely, it can be associated with consumptive coagulopathy due to disseminated intravascular coagulation eventually leading to thrombocytopenia and microangiopathic hemolytic anemia. This specific manifestation is termed Kasabach-Merritt syndrome.
