Retransplantation after kidney graft loss due to polyoma BK virus nephropathy: successful outcome without original allograft nephrectomy

Ginevri, Fabrizio; Pastorino, Nadia; Santis, Riccardo De; Fontana, I.; Sementa, Angela Rita; Losurdo, Giuseppe; Santopietro, Angelo; Perfumo, Francesco; Locatelli, Franco; Maccario, Rita; Azzi, Alberta; Comoli, Patrizia

doi:10.1016/s0272-6386(03)00869-2

Cited by 54 publications

(41 citation statements)

References 13 publications

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“…The apparent contrast of our data to a previous observation (12), reporting the onset of PVAN and graft loss in the only 2 patients, of 15 analyzed, with detectable BKV-specific CD8+ T-cell responses in the peripheral blood, may be explained by sampling times. Indeed, in a patient who lost the graft to PVAN in our historical cohort (13), emergence of BKV-directed cellular immunity was observed, coincident with a therapeutic reduction in maintenance immunosuppression, that could not influence graft outcome in an advanced stage of kidney damage (26). Our study suggests that emergence of BKV-specific immune response in viremic patients without kidney involvement leads to viral clearance and optimal transplant outcome.…”

Section: Ginevri Et Almentioning

confidence: 65%

Prospective Monitoring of Polyomavirus BK Replication and Impact of Pre-Emptive Intervention in Pediatric Kidney Recipients

Ginevri

Azzi

Hirsch

et al. 2007

American Journal of Transplantation

221

222

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Polyoma BK virus (BKV)-associated nephropathy (PVAN) is a relevant cause of poor renal allograft survival.In a prospective analysis, we monitored BKV DNA in blood and urine samples from 62 consecutive pediatric kidney recipients. In patients with BKV replication, we analyzed the impact of reduction of maintenance immunosuppression on viral load kinetics and PVAN in patients with BKV replication. BKV-specific immunity was concomitantly evaluated on blood samples of viremic patients, by measuring the frequency of BKV-specific interferon-c -producing and cytotoxic T cells, and BKV IgG antibody levels. At a median follow-up of 24 months, BK viruria was observed in 39 of 62 patients, while BK viremia developed in 13 patients (21%). In all viremic patients, immunosuppression reduction resulted in the clearance of viremia, and prevented development of PVAN, without increasing the rate of acute rejection or causing graft dysfunction. As a consequence of immunosuppression adjustment, an expansion of BKV-specific cellular immunity was observed that coincided with viral clearance. We conclude that treating pediatric kidney transplant patients pre-emptively with immunosuppression reduction guided by BKV DNA in blood is safe and effective to prevent onset of PVAN. BKV-specific cellular immunity may be useful to guide this intervention.

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Section: Ginevri Et Almentioning

confidence: 65%

Prospective Monitoring of Polyomavirus BK Replication and Impact of Pre-Emptive Intervention in Pediatric Kidney Recipients

Ginevri

Azzi

Hirsch

et al. 2007

American Journal of Transplantation

221

222

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“…Tubulointerstitial damage from direct and indirect effects of the virus and rejection after immunosuppression reduction lead to early graft loss or chronic dysfunction (46,48,51,53,80,86,94,95,124). In recipients who have advanced kidney disease or who have returned to dialysis from BKV nephropathy, retransplantation has been successful (125)(126)(127)(128)(129)(130). In most cases, transplant nephrectomy and/or studies to confirm no active viral replication have been performed.…”

Section: Retransplantationmentioning

confidence: 99%

“…In the setting of active viral replication, it seems prudent. Evidence of BKV-specific immunity can be evaluated before retransplantation (125) but in the setting of a resolved infection can be inferred. However, for preemptive transplantation in recipients of combined organ transplants, for whom reduction in immunosuppression is limited, evidence of no active viral replication or BKV-specific immunity should be determined.…”

Section: Retransplantationmentioning

confidence: 99%

BK Virus Nephropathy and Kidney Transplantation

Bohl

Brennan

2007

Clinical Journal of the American Society of Nephrology

222

175

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Nephropathy from BK virus (BKV) infection is an evolving challenge in kidney transplant recipients. It is the consequence of modern potent immunosuppression aimed at reducing acute rejection and improving allograft survival. Untreated BKV infections lead to kidney allograft dysfunction or loss. Decreased immunosuppression is the principle treatment but predisposes to acute and chronic rejection. Screening protocols for early detection and prevention of symptomatic BKV nephropathy have improved outcomes. Although no approved antiviral drug is available, leflunomide, cidofovir, quinolones, and intravenous Ig have been used. Retransplantation after BKV nephropathy has been successful.Clin J Am Soc Nephrol 2: S36 -S46, 2007. doi: 10.2215/CJN.00920207 P olyomavirus infection in kidney transplant recipients is of increasing interest and research. Although the two human polyomaviruses, BK virus (BKV) and JC virus (JCV), were reported in 1971 (1,2), their influence and importance were limited. The emergence of polyomavirus nephropathy has coincided with the use of new potent immunosuppressive medications (3,4). It is usually associated with BKV, affects up to 8% of recipients, and frequently results in allograft loss or permanent dysfunction (5). It presents as an asymptomatic gradual rise in creatinine with a tubulointerstitial nephritis that mimics rejection, producing a treatment dilemma. The decrease in immunosuppression that is needed to treat infection is opposite to the increases that are needed to treat rejection.Two studies in kidney transplant recipients who were treated with prednisone and azathioprine in the early 1980s have provided the foundation for much of our current understanding of polyomaviruses in transplant recipients. Hogan et al. (6) and Gardner et al. (7) found that the pretransplantation seroprevalence was 80 to 88% for BKV and 54 to 55% for JCV. The posttransplantation rates of polyomavirus infection were 18 to 44% for BKV and 30 to 35% for JCV. Most polyomavirus infections were asymptomatic and occurred within the first 3 mo after transplantation. BKV infection was associated with a rising creatinine. More than 20 yr ago, Gardner et al. (7) warned, "The detection of polyomavirus infection is important as increased immunosuppression needs to be avoided to prevent possible complications."

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“…Nakil öncesi BKV bağışıklığı ve yanıtı değerlendirilmelidir. 80 Tekrar böbrek yetmezliği gelişen ve diyaliz tedavisi başlanan BKVN hastalarında yeniden böbrek nakli başarılı olabilmektedir. [81][82][83] Çoğu olguda greft nefrektomisinden sonra virüsün aktivasyonunun kaybolduğu görülmüştür.…”

Section: Yeni̇den Böbrek Nakli̇unclassified

BK Nephropathy in Renal Transplant Patients: Review

Ayar¹,

Muti²

2014

Turkiye Klinikleri J Nephrol

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38Böbrek Nakilli Hastalarda BK Nefropatisi Ö ÖZ ZE ET T Polyomavirüse bağlı nefropatinin en önemli nedeni insan BK polyomavirüsü (BKV)'dür. Virüs, üriner sistemde latent olarak yaşayabilir. Özellikle solid organ nakli sonrası ve immün sistemi bozulmuş kişilerde aktive olmaktadır. BK ilişkili nefropati (BKVN) böbrek nakli sonrası %1-10 sıklığında görülmekte ve %30-80 greft kaybına ilerlemektedir. BKVN'nin patogenezi tam bilinmemekle birlikte; viral replikasyon ve immünsupresyon suçlanmaktadır. İmmünsupresif protokollerdeki farklılıklar BKVN gelişimini etkileyebilmektedir. Özellikle kalsinörin inhibitörü, mikofenolat mofetil ve steroid içeren üçlü protokollerde risk daha fazladır. Hastalık, böbrek nakli sonrası erken dönemde greft kaybına yol açabilmektedir. Bu nedenle, naklin ilk yılında BKV'nin idrarda veya serumda replikasyonunun izlenmesi hastalığın seyri açısından önemlidir. İmmünsupre-sif tedavinin değiştirilmesi ve antiviral tedaviler, hastalarda virüse karşı hücresel yanıtı arttırmakta ve virüsün çoğalmasını azaltmaktadır. Geç tanı; geriye dönüşümsüz hasara, greft kaybına ve tedavi direncine yol açmaktadır. Sidofovir, leflunomid ve intravenöz immünglobulin gibi yardımcı tedavilerin etkinliği hâlâ tartışma konusudur. Tedaviye rağmen greft kaybı ve diyalize dönüş görüle-bilmektedir. Bu nedenle bu çalışmada, böbrek nakli hastalarında BKVN ile ilgili güncel yaklaşımlara odaklanılmıştır.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : BK virüsü; greft ömrü; böbrek transplantasyonu; immünsupresif ajanlar A AB BS S T TR RA AC CT T The human BK polyomavirus (BKV) is the major cause of polyomavirus-associated nephropathy. The virus can survive latently in urinary system. The virus activates in individuals with impaired immune functions, especially after solid organ transplantation. BK induced nephropathy (BKVN) is seen in 1-10% after kidney transplantation and 30-80% of them progress to graft loss. The pathogenesis of BKVN is unclear, but viral replication and immunosuppression are accused. Differences in immunosuppressive regimens may affect the development of BKVN. Especially, there is more risk in triple protocols including calcineurin inhibitor, mycophenolate mofetil and corticosteroid. The disease leads graft loss in the early period after kidney transplantation. Therefore, the monitoring of replication for BKV in urine or serum is important for disease progression within the first year of transplantation. Changing immunosuppressive and antiviral therapies increase cellular response against the virüs, and decrease viral replication in patients. Late diagnosis causes irreversible damage, treatment resistance and graft loss. The efficacy of adjuvant therapies such as cidofovir, leflunomide and intravenous immunoglobulin are still a matter of debate. Therefore, this review has been focused on the current approaches related with BKVN in kidney transplant patients. K Ke ey y W Wo or rd ds s: : BK virus; graft survival; kidney transplantation; immunosuppressive agents T Tu ur rk ki iy ye e K Kl li in ni ik k...

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Retransplantation after kidney graft loss due to polyoma BK virus nephropathy: successful outcome without original allograft nephrectomy

Cited by 54 publications

References 13 publications

Prospective Monitoring of Polyomavirus BK Replication and Impact of Pre-Emptive Intervention in Pediatric Kidney Recipients

Prospective Monitoring of Polyomavirus BK Replication and Impact of Pre-Emptive Intervention in Pediatric Kidney Recipients

BK Virus Nephropathy and Kidney Transplantation

BK Nephropathy in Renal Transplant Patients: Review

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