Ismael Z. Assi , Shalini Bumb , Shikha Jaiswal , Michelle M. Bryant , Silvi Shah
{"title":"肾移植后急性淋巴细胞增生性疾病","authors":"Ismael Z. Assi , Shalini Bumb , Shikha Jaiswal , Michelle M. Bryant , Silvi Shah","doi":"10.1016/j.xkme.2025.101094","DOIUrl":null,"url":null,"abstract":"<div><div>Posttransplant lymphoproliferative disorder (PTLD) encompasses a spectrum of potentially life-threatening lymphoid proliferations that can arise after solid-organ transplantation, with a bimodal onset typically occurring approximately 12-14 months or approximately 4 years after transplant. Here, we present a novel case of a patient who developed PTLD with an unusually rapid onset, occurring just 7 weeks after receiving a deceased donor kidney transplant. The patient, an Epstein-Barr virus (EBV)-negative recipient of an EBV-positive donor kidney with a complete human leukocyte antigen mismatch, experienced early posttransplant complications including bacteremia and fungemia. These infections, in conjunction with high-risk EBV serostatus and possible underlying genetic susceptibility, may have contributed to uncontrolled B-cell proliferation in the setting of the patient’s impaired immune surveillance. Kidney biopsy confirmed EBV-positive monomorphic diffuse large B-cell lymphoma. The patient was successfully treated with rituximab and reduction of immunosuppression, resulting in resolution of EBV viremia. This case underscores the need to consider PTLD even in the very early posttransplant period, especially in EBV-mismatched recipients, and highlights the complex interplay among infections, immunosuppression, and lymphoproliferative disease pathogenesis.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 10","pages":"Article 101094"},"PeriodicalIF":3.4000,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Acute-Onset Posttransplant Lymphoproliferative Disorder After Kidney Transplant\",\"authors\":\"Ismael Z. Assi , Shalini Bumb , Shikha Jaiswal , Michelle M. Bryant , Silvi Shah\",\"doi\":\"10.1016/j.xkme.2025.101094\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Posttransplant lymphoproliferative disorder (PTLD) encompasses a spectrum of potentially life-threatening lymphoid proliferations that can arise after solid-organ transplantation, with a bimodal onset typically occurring approximately 12-14 months or approximately 4 years after transplant. Here, we present a novel case of a patient who developed PTLD with an unusually rapid onset, occurring just 7 weeks after receiving a deceased donor kidney transplant. The patient, an Epstein-Barr virus (EBV)-negative recipient of an EBV-positive donor kidney with a complete human leukocyte antigen mismatch, experienced early posttransplant complications including bacteremia and fungemia. These infections, in conjunction with high-risk EBV serostatus and possible underlying genetic susceptibility, may have contributed to uncontrolled B-cell proliferation in the setting of the patient’s impaired immune surveillance. Kidney biopsy confirmed EBV-positive monomorphic diffuse large B-cell lymphoma. The patient was successfully treated with rituximab and reduction of immunosuppression, resulting in resolution of EBV viremia. This case underscores the need to consider PTLD even in the very early posttransplant period, especially in EBV-mismatched recipients, and highlights the complex interplay among infections, immunosuppression, and lymphoproliferative disease pathogenesis.</div></div>\",\"PeriodicalId\":17885,\"journal\":{\"name\":\"Kidney Medicine\",\"volume\":\"7 10\",\"pages\":\"Article 101094\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-08-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kidney Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S259005952500130X\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"UROLOGY & NEPHROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kidney Medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S259005952500130X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"UROLOGY & NEPHROLOGY","Score":null,"Total":0}
Acute-Onset Posttransplant Lymphoproliferative Disorder After Kidney Transplant
Posttransplant lymphoproliferative disorder (PTLD) encompasses a spectrum of potentially life-threatening lymphoid proliferations that can arise after solid-organ transplantation, with a bimodal onset typically occurring approximately 12-14 months or approximately 4 years after transplant. Here, we present a novel case of a patient who developed PTLD with an unusually rapid onset, occurring just 7 weeks after receiving a deceased donor kidney transplant. The patient, an Epstein-Barr virus (EBV)-negative recipient of an EBV-positive donor kidney with a complete human leukocyte antigen mismatch, experienced early posttransplant complications including bacteremia and fungemia. These infections, in conjunction with high-risk EBV serostatus and possible underlying genetic susceptibility, may have contributed to uncontrolled B-cell proliferation in the setting of the patient’s impaired immune surveillance. Kidney biopsy confirmed EBV-positive monomorphic diffuse large B-cell lymphoma. The patient was successfully treated with rituximab and reduction of immunosuppression, resulting in resolution of EBV viremia. This case underscores the need to consider PTLD even in the very early posttransplant period, especially in EBV-mismatched recipients, and highlights the complex interplay among infections, immunosuppression, and lymphoproliferative disease pathogenesis.