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Lupus nephritis is the most common organ-threatening manifestation of systemic lupus erythematosus, affecting more than one-third of patients. Induction of remission and maintenance of relapse-free disease have been and continue to be a critical focus of investigation. Because the need for renal replacement therapy in those with an insufficient response to therapy is associated with significantly increased morbidity and mortality, providers and patients are willing to accept moderate to high levels of adverse events associated with treatment. Current standard-of-care regimens for induction and maintenance immunosuppression have led to resumption of adequate renal function and minimization of proteinuria for many patients. Current practice is to maintain maintenance immunosuppression indefinitely for fear of flare upon therapy withdrawal. For those with sustained quiescent disease after several years of maintenance therapy, the risk-to-benefit analysis for ongoing immunosuppression shifts toward an increasing consideration of the adverse effects of immunosuppressive agents. The time has come to begin to study, in a careful and controlled manner, the possibility of withdrawal of immunosuppressant therapy in patients with nephritis who have achieved sustained remission., (Copyright © 2019 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Although the female predominance of autoimmune diseases is not completely understood, sex hormones are thought to play a role. Attention to lifelong reproductive health is especially important for women with autoimmune disorders. Many of these women require long-term immunosuppressive therapy that may affect their ability to clear infections, including viruses, and may alter natural tumor surveillance mechanisms. As a result, women with autoimmune diseases may have different risks for common reproductive-related malignancies that may in turn affect screening guidelines and other preventive measures, including vaccination. Women with autoimmune diseases need to adhere diligently to screening recommendations., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Clostridium difficile is the leading cause of hospital-acquired diarrhea in Europe and North America and is a serious reemerging pathogen. Recent outbreaks have led to increasing morbidity and mortality and have been associated with a new strain (BI/NAP1/027) of C difficile that produces more toxin than historic strains. With the increasing incidence of C difficile infection, clinicians have also seen a change in the epidemiology with increased infections in previously low-risk populations. This chapter highlights the current knowledge on C difficile virulence, human disease, epidemic outbreaks and optimal treatment strategies.

This article describes a transplant recipient with underlying hypocomplementemic urticarial vasculitis syndrome who expressed persistently Epstein-Barr virus nuclear antigen 1 (EBNA1) in peripheral blood. The patient received a bilateral lung transplant and was subsequently followed with monitoring of EBV expression in peripheral blood. Evaluation of viral expression in peripheral blood, serum, and graft tissue was performed with RT-PCR, Q-PCR, indirect immunofluorescence, anti-peptide assays, and in situ hybridization; samples were collected at various time-points up to 91 days post-transplantation. The patient expressed EBNA1 in 8/10 (80%) of the peripheral blood samples tested during the post-transplantation period, and interestingly, even including the day of transplantation. After analyses of indicative EBV mRNA, EBNA1 expression was found mainly to be Qp-initiated EBNA1, known to be important for EBV maintenance. Anti-EBNA1 epitope mapping showed significantly higher and broader antibody responses to EBNA1 epitopes pre-transplantation when compared to normal controls and a matched lung transplant control. Post-transplantation this response was largely diminished but there were still epitopes significantly higher than controls. Our results show the presence of EBV-positive proliferating cells before onset of intensive immunosuppressive treatment. Although no previous connection between EBV and hypocomplementemic urticarial vasculitis syndrome has been reported, it is tempting to speculate that the continuous EBNA1 expression is not caused by immunosuppression or post-transplant lymphoproliferative disease, but may be a factor involved in the etiology of the autoimmune disease.