Nissreen Elfadawy1, Stuart M Flechner, Xiaobo Liu, Jesse Schold, Titte R Srinivas, Emilio Poggio, Richard Fatica, Robin Avery, Sherif B Mossad. 1. 1 Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH. 2 Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH. 3 Division of Nephrology, Medical University of South Carolina, Charleston, SC. 4 Division of Infectious Diseases, Johns Hopkins University, Baltimore, MD. 5 Department of Infectious Disease in the Medicine Institute, Cleveland Clinic, Cleveland, OH. 6 Address correspondence to: Stuart M. Flechner, M.D., F.A.C.S., Glickman Urological and Kidney Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/Q10, Cleveland, OH 44195.
Abstract
BACKGROUND: Cytomegalovirus (CMV) and BK virus (BKV) infections can cause significant morbidity after kidney and kidney-pancreas transplant. There are limited data on the epidemiology and interactions between these two viral pathogens. METHODS: We prospectively screened 609 kidney or kidney-pancreas transplant recipients from January 2007 to June 2011 for BKV and/or CMV viremia. This included 7453 quantitative BKV polymerase chain reaction and 15,496 quantitative CMV polymerase chain reaction tests. We evaluated risk factors and timing of these infections and the impact of treatment of one infection on the other. RESULTS: Among 609 recipients, 108 (17.7%) developed CMV viremia, of which 95 (88%) were asymptomatic, 5 (5%) had CMV syndrome, and 8 (7%) developed CMV tissue invasive disease at a median of 5.6 months after transplantation. Risk factors for CMV infection using multivariable analysis were D+R- serogroup (P≤0.0001), donor age >50 years (P=0.013), and higher mean tacrolimus (P=0.0009) and mycophenolate mofetil (P=0.01) blood levels. The incidence of BKV infection in the total population was 163 of 609 (26.7%), of which 150 (92%) occurred in patents without antecedent CMV viremia. Such patients demonstrated a higher rate of subsequent BKV viremia than patients with antecedent CMV viremia (P=0.003; hazard ratio, 2.05; 95% confidence interval, 1.2-3.4). Moreover, we found that only symptomatic CMV viremia had a significant negative impact on graft survival when compared with asymptomatic CMV viremia and those without CMV viremia (relative risk, 3.5; 95% confidence interval, 1.06-8.9; P=0.04). CONCLUSION: CMV viremia may indirectly protect against subsequent BK viremia possibly due to a reduction of intensity of immunosuppression after diagnosis of CMV viremia.
BACKGROUND: Cytomegalovirus (CMV) and BK virus (BKV) infections can cause significant morbidity after kidney and kidney-pancreas transplant. There are limited data on the epidemiology and interactions between these two viral pathogens. METHODS: We prospectively screened 609 kidney or kidney-pancreas transplant recipients from January 2007 to June 2011 for BKV and/or CMV viremia. This included 7453 quantitative BKV polymerase chain reaction and 15,496 quantitative CMV polymerase chain reaction tests. We evaluated risk factors and timing of these infections and the impact of treatment of one infection on the other. RESULTS: Among 609 recipients, 108 (17.7%) developed CMV viremia, of which 95 (88%) were asymptomatic, 5 (5%) had CMV syndrome, and 8 (7%) developed CMV tissue invasive disease at a median of 5.6 months after transplantation. Risk factors for CMV infection using multivariable analysis were D+R- serogroup (P≤0.0001), donor age >50 years (P=0.013), and higher mean tacrolimus (P=0.0009) and mycophenolate mofetil (P=0.01) blood levels. The incidence of BKV infection in the total population was 163 of 609 (26.7%), of which 150 (92%) occurred in patents without antecedent CMV viremia. Such patients demonstrated a higher rate of subsequent BKV viremia than patients with antecedent CMV viremia (P=0.003; hazard ratio, 2.05; 95% confidence interval, 1.2-3.4). Moreover, we found that only symptomatic CMV viremia had a significant negative impact on graft survival when compared with asymptomatic CMV viremia and those without CMV viremia (relative risk, 3.5; 95% confidence interval, 1.06-8.9; P=0.04). CONCLUSION:CMV viremia may indirectly protect against subsequent BK viremia possibly due to a reduction of intensity of immunosuppression after diagnosis of CMV viremia.
Authors: Nissreen Elfadawy; Stuart M Flechner; Jesse D Schold; Titte R Srinivas; Emilio Poggio; Richard Fatica; Robin Avery; Sherif B Mossad Journal: Clin J Am Soc Nephrol Date: 2014-01-09 Impact factor: 8.237
Authors: Priya S Verghese; David O Schmeling; Jennifer A Knight; Arthur J Matas; Henry H Balfour Journal: Transplantation Date: 2015-03 Impact factor: 4.939
Authors: Darlene Vigil; Nikifor K Konstantinov; Marc Barry; Antonia M Harford; Karen S Servilla; Young Ho Kim; Yijuan Sun; Kavitha Ganta; Antonios H Tzamaloukas Journal: World J Transplant Date: 2016-09-24
Authors: Arturo Blazquez-Navarro; Chantip Dang-Heine; Nicole Wittenbrink; Chris Bauer; Kerstin Wolk; Robert Sabat; Timm H Westhoff; Birgit Sawitzki; Petra Reinke; Oliver Thomusch; Christian Hugo; Michal Or-Guil; Nina Babel Journal: EBioMedicine Date: 2018-07-30 Impact factor: 8.143