Haematological disorders following kidney transplantation

Abstract

Transplantation offers cure for some haematological cancers, end-stage organ failure, but at the cost of long-term complications. Renal transplantation is the best-known kidney replacement therapy and it can prolong end-stage renal disease patient lives for decades. However, patients after renal transplantation are at a higher risk of developing different complications connected not only with surgical procedure but also with immunosuppressive treatment, chronic kidney disease progression and rejection processes. Various blood disorders can develop in post-transplant patients ranging from relatively benign anaemia through cytopenias to therapy-related myelodysplasia and acute myeloid leukaemia (AML) and post-transplant lymphoproliferative disorders followed by a rare and fatal condition of thrombotic microangiopathy and haemophagocytic syndrome. So far literature mainly focused on the post-transplant lymphoproliferative disease. In this review, a variety of haematological problems after transplantation ranging from rare disorders such as myelodysplasia and AML to relatively common conditions such as anaemia and iron deficiency are presented with up-to-date diagnosis and management.

Immune thrombocytopenia secondary to primary cytomegalovirus infection after renal transplantation treated with a thrombopoietin receptor agonist: a case report

“…Thrombocytopenia after RT is developed in up to 30% of RT recipients and often accompanied by cytopenia in other cell lineages. Thrombocytopenia is often observed in the rst year after RT and has a wide variety of causes, including blood disorders (such as haemophagocytic syndrome and thrombotic microangiopathy), viral infections (such as CMV and EBV), immunosuppressants (such as MMF and mTOR inhibitors), and antiviral agents (such as GCV and VGCV) [12]. mTOR inhibitor-induced thrombocytopenia often occurs simultaneously with leukopenia, and usually resolves spontaneously [13].…”

Epos EPO

“…Bei doch bestehendem Substitutionsbedarf gibt es Hinweise, dass die vollständige Korrektur der renalen Anämie in den Referenzbereich Nierengesunder im langfristigen Verlauf sogar zu einem verzögerten Nierenfunktionsverlust sowie einer verbesserten Lebensqualität führen könnte 19 , 20 . Auf Basis dieser Ergebnisse könnten Empfehlungen zu höheren Hämoglobinzielwerten von 12–13 g/dl für nierentransplantierte Patient*innen getriggert werden 21 . Allerdings ist die bisherige Datenlage limitiert und explizite Leitlinien fehlen: In der KDIGO-Leitlinie zur Behandlung transplantierter Patient*innen wird orientierend auf die Leitlinie zur Therapie der Anämie bei Patienten mit CKD verwiesen 22 .…”

“…kontrovers: Auch wenn eine EPO-Substitution den Bedarf an Transfusionen zu reduzieren vermag und möglicherweise zu einer Verbesserung der Lebensqualität führt, ist diese Therapieoption mit einer erhöhten Mortalität und einer höheren Rate an thrombembolischen Komplikationen assoziiert[14,15]. Da der EPO-Signalweg in zelluläre Prozesse wie Differenzierung, Proliferation und Apoptose eingreift, ist ent*innen getriggert werden[21]. Allerdings ist die bisherige Datenlage limitiert und explizite Leitlinien fehlen: In der KDIGO-Leitlinie zur Behandlung transplantierter Patient*innen wird orientierend auf die Leitlinie zur Therapie der Anämie bei Patienten mit CKD verwiesen[22].…”

Unusual presentation of extranodal diffuse large B-cell lymphoma in a solid-organ recipient during long-term immunosuppressive treatment

“…Posttransplant lymphoproliferative disorders (PTLDs) refer to a group of diseases, including diffuse large B-cell lymphoma (DLBCL), that develop after solid organ transplantation and hematopoietic stem cell transplantation (HSCT), resulting in an increased risk of morbidity and mortality and representing the second most common malignancy after skin cancer in transplant recipients. 1,2 The 2017 World Health Organization classification recognizes four PTLD subtypes: nondestructive PTLDs (plasmacytic hyperplasia, infectious mononucleosis, florid follicular hyperplasia), polymorphic PTLDs, monomorphic PTLDs (B cell, T cell, and NK cell, further classified according to the lymphoma they resemble), and classic Hodgkin lymphoma PTLD. 3 The majority of PTLD cases (>85%) are usually observed in the first year posttransplant.…”

“…4 In detail, the cumulative dose of all immunosuppressants is mostly involved in the development of late-onset PTLD, while the EBV genome is found in the majority (>90%) of B-cell PTLDs that occur early after solid organ transplantation. 1,5 Chronic antigenic stimulation by the allograft could have a role in development of EBV-negative PTLD, although the exact physiopathologic mechanisms and cellular genetic changes are complex and largely unknown. 5,6 Extranodal involvement in PTLDs is common, mostly including gastrointestinal tract, lungs, skin, bone marrow, and central nervous system (CNS).…”