Management and Outcome of BK Viremia in Renal Transplant Recipients

Sood, Puneet; Senanayake, Shamila; Sujeet, Kumar; Medipalli, Radhika; Zhu, Yuanfeng; Johnson, Christopher P.; Hariharan, Sundaram

doi:10.1097/tp.0b013e31826690c6

Cited by 91 publications

(103 citation statements)

References 26 publications

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“…Because timely reduction of immunosuppression is the only effective treatment to date (11,12), all recipients are currently screened for BKPyV viremia on a regular basis after transplantation (10)(11)(12)16). Only a subset of recipients, however, is at risk of developing BKPyV viremia (15-30%) and, subsequently, BKPyVAN (1-10%) (10,(12)(13)(14)(15)(16). Apart from rejection treatment following transplantation, pretransplantation risk factors for BKPyV viremia and BKPyVAN have not been identified; therefore, no markers are available to predict which recipients are actually at risk.…”

Section: Discussionmentioning

confidence: 99%

“…BKPyV infection is observed in approximately half of kidney transplant recipients by detection of BKPyV DNA in urine (viruria) (10,(12)(13)(14)(15). In a subset of viruric recipients (15-30% of the total number of recipients), viral DNA is detected in the circulation (viremia); of these viremic recipients, a small proportion (1-10% of all recipients) develops BKPyVAN, ultimately causing allograft failure (10,(12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

“…In a subset of viruric recipients (15-30% of the total number of recipients), viral DNA is detected in the circulation (viremia); of these viremic recipients, a small proportion (1-10% of all recipients) develops BKPyVAN, ultimately causing allograft failure (10,(12)(13)(14)(15)(16). Sustained viremia and BKPyV loads >10 4 genome copies per milliliter (c/mL) are associated with BKPyVAN development (1,2,10).…”

Section: Introductionmentioning

confidence: 99%

“…Sustained viremia and BKPyV loads >10 4 genome copies per milliliter (c/mL) are associated with BKPyVAN development (1,2,10). To identify this subgroup of recipients at risk who require tapering of immunosuppression (14,17), most kidney transplantation centers regularly evaluate recipients currently for detectable BKPyV DNA in blood (10)(11)(12)16). …”

Section: Introductionmentioning

confidence: 99%

“…Reduction of immunosuppressive therapy is the only effective evidence-based treatment to date (11,12).…”

Section: Introductionmentioning

confidence: 99%

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Pretransplantation Donor–Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation

Wunderink

Meijden

Brouwer

et al. 2017

American Journal of Transplantation

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Kidney transplant donors are not currently implicated in predicting BK polyomavirus (BKPyV) infection in kidney transplant recipients. It has been postulated, however, that BKPyV infection originates from the kidney allograft. Because BKPyV seroreactivity correlates with BKPyV replication and thus might mirror the infectious load, we investigated whether BKPyV seroreactivity of the donor predicts viremia and BKPyV‐associated nephropathy (BKPyVAN) in the recipient. In a retrospective cohort of 407 living kidney donor–recipient pairs, pretransplantation donor and recipient sera were tested for BKPyV IgG levels and correlated with the occurrence of recipient BKPyV viremia and BKPyVAN within 1 year after transplantation. Donor BKPyV IgG level was strongly associated with BKPyV viremia and BKPyVAN (p < 0.001), whereas recipient BKPyV seroreactivity showed a nonsignificant inverse trend. Pairing of high–BKPyV‐seroreactive donors with low‐seroreactive recipients resulted in a 10‐fold increased risk of BKPyV viremia (hazard ratio 10.1, 95% CI 3.5–29.0, p < 0.001). In multivariate analysis, donor BKPyV seroreactivity was the strongest pretransplantation factor associated with viremia (p < 0.001) and BKPyVAN (p = 0.007). The proportional relationship between donor BKPyV seroreactivity and recipient infection suggests that donor BKPyV seroreactivity reflects the infectious load of the kidney allograft and calls for the use of pretransplantation BKPyV serological testing of (potential) donors and recipients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Reduction of immunosuppressive therapy is the only effective evidence-based treatment to date (11,12).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Pretransplantation Donor–Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation

Wunderink

Meijden

Brouwer

et al. 2017

American Journal of Transplantation

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BK and JC polyomavirus infections in Tunisian renal transplant recipients

Boukoum¹,

Nahdi²,

Sahtout

et al. 2015

J. Med. Virol.

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The aim of this prospective study was to investigate the rate of BK (BKPyV) and JC (JCPyV) polyomavirus infections and their influence on allograft function in Tunisian renal transplant recipients. A total of 72 renal transplant recipients were studied. BKPyV and JCPyV were detected and quantified by real-time PCR in urine and plasma. Demographic and laboratory characteristics were collected for each patient. Polyomavirus DNAuria was detected in 54 (75%) of renal transplant recipients: 26 (36%) had BKPyV DNAuria, 20 (28%) had JCPyV DNAuria, and 8 (11%) had a dual BKPyV/JCPyV DNAuria. BKPyV DNAemia was detected in four (5.5%) patients, whereas no patient had JCPyV viremia. More than 70% of BKPyV and JCPyV infections started within the first 3 months post-transplant. The risk for positive DNAemia was observed in patients with DNAuria level >10(7) copies/ml. BK Polyomavirus-associated nephropathy (BKPyVAN) was observed in two patients. This study highlights the high frequency of BKPyV and JCPyV viruria during the first year post-transplant with the highest incidence observed in the third month. We identified several risk factors that were associated with BKV DNAuria including age, sex of patients, and the use of tacrolimus instead of cyclosporine A at month 3. The use of cyclosporine A instead of tacrolimus was identified as risk factor for JCV viruria in month 3. No statistical difference in the allograft function was found between BKPyV and/or JCPyV infected and uninfected patients.

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Impact of HPyV9 and TSPyV coinfection on the development of BK polyomavirus viremia and associated nephropathy after kidney transplantation

Rijn

Wunderink

Brouwer

et al. 2019

Journal of Medical Virology

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Background BK polyomavirus (BKPyV) persistently infects the urinary tract and causes viremia and nephropathy in kidney transplantation (KTx), recipients. In a previous study, we observed an increased incidence and load of BKPyV viremia in KTx patients coinfected with human polyomavirus 9 (HPyV9). Here we sought confirmation of this observation and explored whether novel HPyVs that have been detected in urine (HPyV9 and trichodysplasia spinulosa polyomavirus [TSPyV]) potentially aggravate BKPyV infection. Methods A well‐characterized cohort of 209 KTx donor‐recipient pairs was serologically and molecularly analyzed for HPyV9 and TSPyV coinfection. These data were correlated with the occurrence of BKPyV viremia and BKPyVAN in the recipients within a year after KTx. Results Seropositivity for HPyV9 (19%) and TSPyV (89%) was comparable between donors and recipients and did not correlate with BKPyV viremia and BKPyVAN that developed in 25% and 3% of the recipients, respectively. Two recipients developed TSPyV viremia and none HPyV9 viremia. Modification of the predictive effect of donor BKPyV seroreactivity on recipient BKPyV viremia by HPyV9 and TSPyV was not observed. Conclusions Our data provide no evidence for a promoting effect of HPyV9 and TSPyV on BKPyV infection and BKPyVAN in renal allograft patients. Therefore, we do not recommend including HPyV9 and TSPyV screening in KTx patients.

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Management and Outcome of BK Viremia in Renal Transplant Recipients

Abstract: Reduction in immunosuppression alone resulted in the successful resolution of viremia with preservation of renal function and prevention of clinical BKV nephritis and graft loss.

Cited by 91 publications

References 26 publications

Pretransplantation Donor–Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation

Pretransplantation Donor–Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation

BK and JC polyomavirus infections in Tunisian renal transplant recipients

Impact of HPyV9 and TSPyV coinfection on the development of BK polyomavirus viremia and associated nephropathy after kidney transplantation

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