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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Macrophage activation syndrome (MAS), secondary form of hemophagocytic lymphohistiocytosis, is commonly associated with rheumatologic and autoimmune conditions but can be triggered by acute viral infections, classically Epstein Barr Virus, but also Cytomegalovirus (CMV). Uncontrolled activation of CD8+ T cells and macrophages leads to cytokine storm, pancytopenias, and multiorgan failure. Left untreated, MAS carries a high incidence of morbidity and mortality. We present an unexpected occurrence of CMV-related MAS, heralded by acute kidney injury (AKI).
A 38 year-old woman, with end stage renal disease from lupus nephritis, underwent her second kidney transplant, thymoglobulin induction, with immediate allograft function, baseline serum creatinine (SCr) of 1.4-1.6 mg/dL. Her post-transplant course was complicated by antibody mediated rejection 2-months post-transplant, successfully treated with pulse steroids, plasmapheresis, IVIG and rituximab. She was maintained on mycophenolic acid 720 mg twice a day, tacrolimus 2 mg twice a day and prednisone 5 mg daily. Unexpectedly, 5-months post-transplant, she developed an acute febrile illness and cough with hemoptysis, diagnosed with Bordetella pertussis, treated with Azithromycin. She was clinically improving but developed pancytopenia and AKI (SCr 2.95 mg/dL) with new onset proteinuria (UPCR 0.415 mg/mg). Renal transplant biopsy revealed acute endocapillary glomerulonephritis, with renal tubular injury, severe diffuse interstitial and endocapillary inflammation by macrophages, and endothelial swelling with intravascular injury from aggregates of macrophages; electron microscopy showed macrophages with erythrophagocytosis filled glomerular capillary loops. Given the concern for biopsy-proven MAS, empiric pulse steroids were initiated with gradual improvement of serum creatinine. Infectious workup revealed CMV viremia, with initial viral load 2,611 IU/mL, peaking at 15,674 IU/mL. Treatment with IV ganciclovir was initiated, with improvement of pancytopenia. Maintenance valganciclovir was continued and renal function returned to prior baseline.
See above
Macrophage activation syndrome (MAS) is a life-threatening hyperinflammatory condition. Potential pathogenesis of CMV-induced MAS involves viral reactivation leading to excessive cytokine production, including interleukin-6, tumor necrosis factor-alpha, and interferon-gamma. An overwhelming systemic inflammatory response leads to cytokine storm and multiorgan failure. Treatment requires two parallel strategies: rapid immunosuppression and management of the underlying trigger. In our case, allograft dysfunction and pancytopenia heralded the detection of CMV viremia. Targeted anti-viral therapy led to resolution of CMV infection and complete recovery of renal allograft function.
