Post-transplant lymphoproliferative disorder following kidney transplantation: a population-based cohort study

Abstract

SUMMARYPost-transplant lymphoproliferative disorder (PTLD) incidence is difficult to determine, mainly because both early and other lesions may go unrecognized and unregistered. Few studies have included systematic pathology review to maximize case identification and decide more accurately PTLD frequency after long-term post-transplantation follow-up. A retrospective population-based cohort study including all kidney transplant recipients at two Danish centres ; population covered 3.1 million; 2175 transplantations in 1906 patients). Pathology reports were reviewed for all patient biopsies to identify possible PTLDs. Candidate PTLDs underwent histopathological review and classification. Seventy PTLD cases were identified in 2175 transplantations (3.2%). The incidence rate (IR) after first transplantation was 5.4 cases per 1000 patient-years (95% CI: 4.0-7.3). Most PTLDs were monomorphic (58.5%), or early lesions (21.5%). Excluding early lesions and patients <18 years, IR was 3.7 (95% CI: 2.9-5.5). Ten patients with PTLD were retransplanted, 2 developing further PTLDs. Post-transplant patient survival was inferior in patients with PTLD, while death-censored graft survival was not. Using registry data together with extensive pathological review and long follow-up, a rather high incidence of PTLD was found.

Long-lasting chronic high load carriage of Epstein-Barr virus is more common in young pediatric renal transplant recipients

“…Immunosuppression is another risk factor for developing CHL-and EBV-associated PTLD [16,22,25,37]. Thus, the incidence of PTLD is higher in pediatric recipients of heart, lung, and intestinal transplants, traditionally treated with more intense immunosuppression, and lower in pediatric liver and renal recipients, who are treated with less intense immunosuppression [6,17,40].…”

“…High EBV DNA levels have been recognized as a risk factor for developing PTLD in transplant recipients [2,22,45]. However, children may remain in a CHL carrier state without developing PTLD, and high or persistent EBV load alone does not appear to be predictive for development of PTLD in pediatric renal transplant recipients [25,46].…”

“…The risk for PTLD in the pediatric SOT population is highest after intestinal transplantation (26.8%), followed by heart-lung (19.5%), heart (7.7-12.9%), liver (4%), and kidney transplantation (1-7%) [10][11][12][13][14][15][16][17][18]. EBV-associated PTLD in pediatric renal transplant recipients has been associated with graft loss [19] and has a mortality rate of 32-48% [15,20,21].…”

“…According to many studies, important risk factors for PTLD in pediatric graft recipients are the lack of EBV IgG antibodies at the time of transplantation, the overall burden of immunosuppressive therapy, the presence of a concomitant primary cytomegalovirus (CMV) infection and high EBV DNA levels in blood [7,14,16,[22][23][24]. However, in other studies, transplant recipients have been observed to display high EBV loads without developing PTLD [25,26].…”

Primary central nervous system post-transplant lymphoproliferative disorders: the spectrum of imaging appearances and differential

“…Central nervous system post-transplant lymphoproliferative disorder (CNS-PTLD) is a rare disorder due to immunosuppression secondary to solid organ, stem cell, or bone marrow transplantation [1,2]. Cases begin to appear as early as 6 weeks in the first year after transplantation but most cases take years to present after transplantation and the attendant immunosuppression.…”