The patient continued on dual immunosuppressive therapy thereafter and there were no episodes of acute rejection

The patient continued on dual immunosuppressive therapy thereafter and there were no episodes of acute rejection. associated with post-transplant EBV contamination, of broad interest to transplant physicians, haematologists, and microbiologists, and the effective novel use of monoclonal anti-CD20 therapy. Electronic supplementary material The online version of this article (doi:10.1186/s12882-015-0096-3) contains supplementary material, which is available to authorized users. strong class=”kwd-title” Keywords: EBV, Kidney transplantation, AIHA, Rituximab Background Autoimmune haemolytic anaemia (AIHA) is an immune disease characterised by antibodies directed against autologous red blood cells (RBCs). Typically patients exhibit anaemia with reticulocytosis, spherocytes and polychromasia around the blood film with a positive direct antiglobulin test (DAT) which is the hallmark [1], in addition there is often increased unconjugated serum bilirubin and elevated serum lactate dehydrogenase (LDH). The antibodies can be subdivided into warm or cold agglutinins depending on the thermal range of activity [2] and the subsequent anaemia can be profound and life threatening leading to large transfusion requirements. The aetiology is usually unknown, categorised either as primary (idiopathic) or secondary when associated with malignancy (in particular chronic lymphocytic leukaemia), connective tissue and inflammatory diseases, infections (both viral and mycoplasma associated with a cold AIHA) [2, 3], or drugs (e.g. purine analogues and alkylating brokers) [4, 5]. Alloantibody can also lead to haemolysis post haematopoietic stem cell transplant, solid INH6 organ transplant (i.e. passenger B lymphocyte syndrome), pregnancy and after transfusion [6]. Epstein-Barr computer virus is one of the eight INH6 human herpes viruses, and common in humans. In the United States, by the age of 40 as many as 95?% of adults have been infected with EBV. Infants (after maternal antibody protection has disappeared) and children have asymptomatic or moderate disease. In adolescence or young adults, EBV causes infectious mononucleosis in up to 50?%. Symptoms of infectious mononucleosis are commonly fever, sore throat, and lymphadenopathy and are almost never fatal. EBV then establishes a lifelong dormant contamination in B cells [7]. It is a carcinogenic computer virus associated with Burkitts lymphoma, Hodgkins disease and nasopharyngeal carcinoma [8]. After transplantation EBV disease can present with varied manifestations, including nonspecific febrile illness, gastroenteritis, hepatitis, mimicking other viral infections, and most seriously post-transplant lymphoproliferative disorder (PTLD) [9]. It remains unclear why EBV causes autoimmune disease. IgM antibodies to autoantigens are normally present in the plasma at low non-pathologic titre. It has been suggested that this B-cell clones that normally produce these autoantibodies are altered to produce IgG antibodies in high and pathogenic levels in AIHA [10]. Alternatively, defective control of IgG auto reactivity by autologous IgM [11] or altered T-cell function [12] has been proposed. AIHA after solid organ transplantation has been reported infrequently [13] and usually occurs early in the course [14]. In this report, we describe a severe and late presentation in the context of donor associated EBV viraemia, the treatment and use of novel therapy. Case presentation In January 2013 a 44?year aged white female presented to our institution with malaise, exertional breathlessness, night sweats and a headache. She had received a pre-emptive deceased donor kidney INH6 transplant 5?years earlier. The kidney characteristics were donation after circulatory death [DCD], human leucocyte antigen (HLA) INH6 mismatch A1:B1:DR1, cytomegalovirus (CMV) serology of both donor and recipient were unfavorable but Epstein-Barr computer virus (EBV) serology of the donor was positive whereas the recipient was unfavorable. The aetiology of end stage renal disease was likely congenital, initial presentation was with advanced chronic kidney disease and a single functioning kidney. The only baseline Lamb2 comorbidity was congenital nystagmus. Primary graft function was excellent and stabilised with serum creatinine 90?mol/L [1.0?mg/dL] and eGFR 60?ml/min/1.73?m2. Induction immunosuppression was with basiliximab and maintenance was tacrolimus, mycophenolate mofetil and prednisolone, as per local protocols. She had been treated with valganciclovir for CMV viraemia at 3?months and mycophenolate was electively withdrawn in line with institutional protocol after 7?months. The patient continued.