Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients: A prospective evaluation

Cinthia B. Drachenberg, Hans H. Hirsch, John C. Papadimitriou, Rainer Gosert, Ravinder K. Wali, Raghava Munivenkatappa, Joseph Nogueira, Charles B. Cangro, Abdolreza Haririan, Susan Mendley, Emilio Ramos

Research output: Contribution to journalArticle

Abstract

BACKGROUND. JC virus (JCV) viruria is more common than BK virus (BKV) viruria in healthy individuals but in kidney transplants (KT), polyomavirus nephropathy (PVAN) is primarily caused by BKV. Few cases of PVAN have been attributed to JCV. Systematic studies on JCV replication in KT are lacking. METHODS. Out of a cohort of KT patients screened with urine cytology, patients shedding decoy cells were studied (n=103). Molecular studies demonstrated BKV, JCV, or BKV+JCV shedding in 58 (56.3%), 28 (27.2%), and 17 (16.5%), respectively. Biopsy was performed when decoy cells persisted 2 months or serum creatinine increased >20%. RESULTS. BKV viruria was strongly associated with BKV viremia (93%), PVAN (48%, P=0.01) and graft loss (P=0.03). Higher BKV viremia correlated with graft dysfunction (P=0.01), more advanced histological pattern of PVAN (P93%). JCV viruria, was more often asymptomatic (P=0.002) and affected older patients (P=0.02). JCV PVAN was less common (21.4%) and was characterized by sparse cytopathic changes but significant inflammation and fibrosis. JCV viremia was rare (14.2%), transient, and low (mean 2.0E+03/mL). After reduction of immunosuppression decoy cells persisted in >50% of patients with JCV (P=0.0001), but no graft loss occurred. During the period of the current study, the incidence of BKV-PVAN was 5.5% and the incidence of JCV-PVAN was 0.9%. CONCLUSIONS. The data point to significant differences of BKV and JCV biology regarding replication and disease in KT patients, with important implications for screening and management.

Original languageEnglish (US)
Pages (from-to)323-330
Number of pages8
JournalTransplantation
Volume84
Issue number3
DOIs
StatePublished - Aug 2007
Externally publishedYes

Fingerprint

BK Virus
JC Virus
Kidney
Transplants
Viremia
Transplant Recipients
Virus Shedding
Polyomavirus
Kidney Diseases
Virus Replication
Immunosuppression
Cell Biology
Creatinine
Fibrosis
Cohort Studies

Keywords

  • Decoy cells
  • Polyomavirus nephropathy patterns
  • Screening
  • Viremia
  • Viruria

ASJC Scopus subject areas

  • Transplantation
  • Immunology

Cite this

Drachenberg, C. B., Hirsch, H. H., Papadimitriou, J. C., Gosert, R., Wali, R. K., Munivenkatappa, R., ... Ramos, E. (2007). Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients: A prospective evaluation. Transplantation, 84(3), 323-330. https://doi.org/10.1097/01.tp.0000269706.59977.a5

Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients : A prospective evaluation. / Drachenberg, Cinthia B.; Hirsch, Hans H.; Papadimitriou, John C.; Gosert, Rainer; Wali, Ravinder K.; Munivenkatappa, Raghava; Nogueira, Joseph; Cangro, Charles B.; Haririan, Abdolreza; Mendley, Susan; Ramos, Emilio.

In: Transplantation, Vol. 84, No. 3, 08.2007, p. 323-330.

Research output: Contribution to journalArticle

Drachenberg, CB, Hirsch, HH, Papadimitriou, JC, Gosert, R, Wali, RK, Munivenkatappa, R, Nogueira, J, Cangro, CB, Haririan, A, Mendley, S & Ramos, E 2007, 'Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients: A prospective evaluation', Transplantation, vol. 84, no. 3, pp. 323-330. https://doi.org/10.1097/01.tp.0000269706.59977.a5
Drachenberg CB, Hirsch HH, Papadimitriou JC, Gosert R, Wali RK, Munivenkatappa R et al. Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients: A prospective evaluation. Transplantation. 2007 Aug;84(3):323-330. https://doi.org/10.1097/01.tp.0000269706.59977.a5
Drachenberg, Cinthia B. ; Hirsch, Hans H. ; Papadimitriou, John C. ; Gosert, Rainer ; Wali, Ravinder K. ; Munivenkatappa, Raghava ; Nogueira, Joseph ; Cangro, Charles B. ; Haririan, Abdolreza ; Mendley, Susan ; Ramos, Emilio. / Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients : A prospective evaluation. In: Transplantation. 2007 ; Vol. 84, No. 3. pp. 323-330.
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abstract = "BACKGROUND. JC virus (JCV) viruria is more common than BK virus (BKV) viruria in healthy individuals but in kidney transplants (KT), polyomavirus nephropathy (PVAN) is primarily caused by BKV. Few cases of PVAN have been attributed to JCV. Systematic studies on JCV replication in KT are lacking. METHODS. Out of a cohort of KT patients screened with urine cytology, patients shedding decoy cells were studied (n=103). Molecular studies demonstrated BKV, JCV, or BKV+JCV shedding in 58 (56.3{\%}), 28 (27.2{\%}), and 17 (16.5{\%}), respectively. Biopsy was performed when decoy cells persisted 2 months or serum creatinine increased >20{\%}. RESULTS. BKV viruria was strongly associated with BKV viremia (93{\%}), PVAN (48{\%}, P=0.01) and graft loss (P=0.03). Higher BKV viremia correlated with graft dysfunction (P=0.01), more advanced histological pattern of PVAN (P93{\%}). JCV viruria, was more often asymptomatic (P=0.002) and affected older patients (P=0.02). JCV PVAN was less common (21.4{\%}) and was characterized by sparse cytopathic changes but significant inflammation and fibrosis. JCV viremia was rare (14.2{\%}), transient, and low (mean 2.0E+03/mL). After reduction of immunosuppression decoy cells persisted in >50{\%} of patients with JCV (P=0.0001), but no graft loss occurred. During the period of the current study, the incidence of BKV-PVAN was 5.5{\%} and the incidence of JCV-PVAN was 0.9{\%}. CONCLUSIONS. The data point to significant differences of BKV and JCV biology regarding replication and disease in KT patients, with important implications for screening and management.",
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T1 - Polyomavirus BK versus JC replication and nephropathy in renal transplant recipients

T2 - A prospective evaluation

AU - Drachenberg, Cinthia B.

AU - Hirsch, Hans H.

AU - Papadimitriou, John C.

AU - Gosert, Rainer

AU - Wali, Ravinder K.

AU - Munivenkatappa, Raghava

AU - Nogueira, Joseph

AU - Cangro, Charles B.

AU - Haririan, Abdolreza

AU - Mendley, Susan

AU - Ramos, Emilio

PY - 2007/8

Y1 - 2007/8

N2 - BACKGROUND. JC virus (JCV) viruria is more common than BK virus (BKV) viruria in healthy individuals but in kidney transplants (KT), polyomavirus nephropathy (PVAN) is primarily caused by BKV. Few cases of PVAN have been attributed to JCV. Systematic studies on JCV replication in KT are lacking. METHODS. Out of a cohort of KT patients screened with urine cytology, patients shedding decoy cells were studied (n=103). Molecular studies demonstrated BKV, JCV, or BKV+JCV shedding in 58 (56.3%), 28 (27.2%), and 17 (16.5%), respectively. Biopsy was performed when decoy cells persisted 2 months or serum creatinine increased >20%. RESULTS. BKV viruria was strongly associated with BKV viremia (93%), PVAN (48%, P=0.01) and graft loss (P=0.03). Higher BKV viremia correlated with graft dysfunction (P=0.01), more advanced histological pattern of PVAN (P93%). JCV viruria, was more often asymptomatic (P=0.002) and affected older patients (P=0.02). JCV PVAN was less common (21.4%) and was characterized by sparse cytopathic changes but significant inflammation and fibrosis. JCV viremia was rare (14.2%), transient, and low (mean 2.0E+03/mL). After reduction of immunosuppression decoy cells persisted in >50% of patients with JCV (P=0.0001), but no graft loss occurred. During the period of the current study, the incidence of BKV-PVAN was 5.5% and the incidence of JCV-PVAN was 0.9%. CONCLUSIONS. The data point to significant differences of BKV and JCV biology regarding replication and disease in KT patients, with important implications for screening and management.

AB - BACKGROUND. JC virus (JCV) viruria is more common than BK virus (BKV) viruria in healthy individuals but in kidney transplants (KT), polyomavirus nephropathy (PVAN) is primarily caused by BKV. Few cases of PVAN have been attributed to JCV. Systematic studies on JCV replication in KT are lacking. METHODS. Out of a cohort of KT patients screened with urine cytology, patients shedding decoy cells were studied (n=103). Molecular studies demonstrated BKV, JCV, or BKV+JCV shedding in 58 (56.3%), 28 (27.2%), and 17 (16.5%), respectively. Biopsy was performed when decoy cells persisted 2 months or serum creatinine increased >20%. RESULTS. BKV viruria was strongly associated with BKV viremia (93%), PVAN (48%, P=0.01) and graft loss (P=0.03). Higher BKV viremia correlated with graft dysfunction (P=0.01), more advanced histological pattern of PVAN (P93%). JCV viruria, was more often asymptomatic (P=0.002) and affected older patients (P=0.02). JCV PVAN was less common (21.4%) and was characterized by sparse cytopathic changes but significant inflammation and fibrosis. JCV viremia was rare (14.2%), transient, and low (mean 2.0E+03/mL). After reduction of immunosuppression decoy cells persisted in >50% of patients with JCV (P=0.0001), but no graft loss occurred. During the period of the current study, the incidence of BKV-PVAN was 5.5% and the incidence of JCV-PVAN was 0.9%. CONCLUSIONS. The data point to significant differences of BKV and JCV biology regarding replication and disease in KT patients, with important implications for screening and management.

KW - Decoy cells

KW - Polyomavirus nephropathy patterns

KW - Screening

KW - Viremia

KW - Viruria

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