Sami Alasfar1,2, Isaac E Hall3, Sherry G Mansour4,5, Yaqi Jia6, Heather R Thiessen-Philbrook6, Francis L Weng7, Pooja Singh8, Bernd Schröppel9, Thangamani Muthukumar10,11, Sumit Mohan12,13, Rubab F Malik6, Meera N Harhay14,15, Mona D Doshi16, Enver Akalin17, Jonathan S Bromberg18,19, Daniel C Brennan6, Peter P Reese20,21,22, Chirag R Parikh6. 1. Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. salasfa1@jhmi.edu. 2. Johns Hopkins School of Medicine, 1830 E. Monument St., Suite 416, Baltimore, MD, 21287, USA. salasfa1@jhmi.edu. 3. Department of Internal Medicine, Division of Nephrology & Hypertension, University of Utah School of Medicine, Salt Lake City, UT, USA. 4. Program of Applied Translational Research, Yale University School of Medicine, New Haven, CT, USA. 5. Department of Internal Medicine, Section of Nephrology, Yale University School of Medicine, New Haven, CT, USA. 6. Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 7. Saint Barnabas Medical Center, RWJ Barnabas Health, Livingston, NJ, USA. 8. Department of Medicine, Division of Nephrology, Sidney Kimmel Medical College, Thomas Jefferson University Hospital, Philadelphia, PA, USA. 9. Section of Nephrology, University of Ulm, Ulm, Germany. 10. Department of Medicine, Division of Nephrology and Hypertension, New York Presbyterian Hospital-Weill Cornell Medical Center, New York, NY, USA. 11. Department of Transplantation Medicine, New York Presbyterian Hospital-Weill Cornell Medical Center, New York, NY, USA. 12. Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA. 13. Department of Medicine, Division of Nephrology, Columbia University Vagelos College of Physicians & Surgeons, New York, NY, USA. 14. Department of Medicine, Drexel University College of Medicine, Philadelphia, PA, USA. 15. Department of Epidemiology and Biostatistics, Drexel University Dornsife School of Public Health, Philadelphia, PA, USA. 16. Department of Internal Medicine, Division of Nephrology, University of Michigan Medical School, Ann Arbor, MI, USA. 17. Kidney Transplant Program, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA. 18. Department of Surgery, Division of Transplantation, University of Maryland School of Medicine, Baltimore, MD, USA. 19. Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA. 20. Department of Medicine, Renal-Electrolyte and Hypertension Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. 21. Department of Biostatistics, Epidemiology & Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. 22. Department of Medical Ethics and Health Policy, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Abstract
BACKGROUND: Post-Transplant erythrocytosis (PTE) has not been studied in large recent cohorts. In this study, we evaluated the incidence, risk factors, and outcome of PTE with current transplant practices using the present World Health Organization criteria to define erythrocytosis. We also tested the hypothesis that the risk of PTE is greater with higher-quality kidneys. METHODS: We utilized the Deceased Donor Study which is an ongoing, multicenter, observational study of deceased donors and their kidney recipients that were transplanted between 2010 and 2013 across 13 centers. Eryrthocytosis is defined by hemoglobin> 16.5 g/dL in men and> 16 g/dL in women. Kidney quality is measured by Kidney Donor Profile Index (KDPI). RESULTS: Of the 1123 recipients qualified to be in this study, PTE was observed at a median of 18 months in 75 (6.6%) recipients. Compared to recipients without PTE, those with PTE were younger [mean 48±11 vs 54±13 years, p < 0.001], more likely to have polycystic kidney disease [17% vs 6%, p < 0.001], have received kidneys from younger donors [36 ±13 vs 41±15 years], and be on RAAS inhibitors [35% vs 22%, p < 0.001]. Recipients with PTE were less likely to have received kidneys from donors with hypertension [16% vs 32%, p = 0.004], diabetes [1% vs 11%, p = 0.008], and cerebrovascular event (24% vs 36%, p = 0.036). Higher KDPI was associated with decreased PTE risk [HR 0.98 (95% CI: 0.97-0.99)]. Over 60 months of follow-up, only 17 (36%) recipients had sustained PTE. There was no association between PTE and graft failure or mortality, CONCLUSIONS: The incidence of PTE was low in our study and PTE resolved in majority of patients. Lower KDPI increases risk of PTE. The underutilization of RAAS inhibitors in PTE patients raises the possibility of under-recognition of this phenomenon and should be explored in future studies.
BACKGROUND: Post-Transplant erythrocytosis (PTE) has not been studied in large recent cohorts. In this study, we evaluated the incidence, risk factors, and outcome of PTE with current transplant practices using the present World Health Organization criteria to define erythrocytosis. We also tested the hypothesis that the risk of PTE is greater with higher-quality kidneys. METHODS: We utilized the Deceased Donor Study which is an ongoing, multicenter, observational study of deceased donors and their kidney recipients that were transplanted between 2010 and 2013 across 13 centers. Eryrthocytosis is defined by hemoglobin> 16.5 g/dL in men and> 16 g/dL in women. Kidney quality is measured by Kidney Donor Profile Index (KDPI). RESULTS: Of the 1123 recipients qualified to be in this study, PTE was observed at a median of 18 months in 75 (6.6%) recipients. Compared to recipients without PTE, those with PTE were younger [mean 48±11 vs 54±13 years, p < 0.001], more likely to have polycystic kidney disease [17% vs 6%, p < 0.001], have received kidneys from younger donors [36 ±13 vs 41±15 years], and be on RAAS inhibitors [35% vs 22%, p < 0.001]. Recipients with PTE were less likely to have received kidneys from donors with hypertension [16% vs 32%, p = 0.004], diabetes [1% vs 11%, p = 0.008], and cerebrovascular event (24% vs 36%, p = 0.036). Higher KDPI was associated with decreased PTE risk [HR 0.98 (95% CI: 0.97-0.99)]. Over 60 months of follow-up, only 17 (36%) recipients had sustained PTE. There was no association between PTE and graft failure or mortality, CONCLUSIONS: The incidence of PTE was low in our study and PTE resolved in majority of patients. Lower KDPI increases risk of PTE. The underutilization of RAAS inhibitors in PTE patients raises the possibility of under-recognition of this phenomenon and should be explored in future studies.
Authors: B A Julian; R R Brantley; C V Barker; T Stopka; R S Gaston; J J Curtis; J Y Lee; J T Prchal Journal: J Am Soc Nephrol Date: 1998-06 Impact factor: 10.121
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Authors: Vishnu S Potluri; Chirag R Parikh; Isaac E Hall; Joseph Ficek; Mona D Doshi; Isabel Butrymowicz; Francis L Weng; Bernd Schröppel; Heather Thiessen-Philbrook; Peter P Reese Journal: Clin J Am Soc Nephrol Date: 2015-12-14 Impact factor: 8.237