Long-Term Results of Pancreas Transplantation Under Tacrolimus Immunosuppression1

Jordan, Mark L.; Shapiro, R; Gritsch, H. Albin; Egidi, F.; Khanna, Ajai; Vivas, Carlos; Scantlebury, Velma P.; Fung, John J.; Starzl, Thomas E.; Corry, Robert J.

doi:10.1097/00007890-199901270-00014

Cited by 50 publications

(1 citation statement)

References 25 publications

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“…The mechanisms by which ACE inhibitors and ATII receptor antagonists cause PTA, include inhibition of endogenous erythropoietin production, inhibition of ATII-mediated stimulation of red blood cell precursors (Macdougall, 1999 ), and the generation of an erythropoiesis-inhibiting protein by ACE inhibitors (Henriksen and Jacob, 2003 ). In addition, the application of antiviral (Chhabra et al, 2008 ), antimicrobial (Reindl-Schwaighofer and Oberbauer, 2014 ), and antilymphocyte (Jordan et al, 1999 ) drugs [such as ganciclovir, trimethoprim-sulfamethoxazole, antilymphocyte globulin (ALG)] have been reported to cause PTA in renal transplant recipients.…”

Section: Post-transplant Anemia (Pta)mentioning

confidence: 99%

Blood disorders typically associated with renal transplantation

Yang

Chen³

2015

Front. Cell Dev. Biol.

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Renal transplantation has become one of the most common surgical procedures performed to replace a diseased kidney with a healthy kidney from a donor. It can help patients with kidney failure live decades longer. However, renal transplantation also faces a risk of developing various blood disorders. The blood disorders typically associated with renal transplantation can be divided into two main categories: (1) Common disorders including post-transplant anemia (PTA), post-transplant lymphoproliferative disorder (PTLD), post-transplant erythrocytosis (PTE), and post-transplant cytopenias (PTC, leukopenia/neutropenia, thrombocytopenia, and pancytopenia); and (2) Uncommon but serious disorders including hemophagocytic syndrome (HPS), thrombotic microangiopathy (TMA), therapy-related myelodysplasia (t-MDS), and therapy-related acute myeloid leukemia (t-AML). Although many etiological factors involve the development of post-transplant blood disorders, immunosuppressive agents, and viral infections could be the two major contributors to most blood disorders and cause hematological abnormalities and immunodeficiency by suppressing hematopoietic function of bone marrow. Hematological abnormalities and immunodeficiency will result in severe clinical outcomes in renal transplant recipients. Understanding how blood disorders develop will help cure these life-threatening complications. A potential therapeutic strategy against post-transplant blood disorders should focus on tapering immunosuppression or replacing myelotoxic immunosuppressive drugs with lower toxic alternatives, recognizing and treating promptly the etiological virus, bacteria, or protozoan, restoring both hematopoietic function of bone marrow and normal blood counts, and improving kidney graft survival.

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