Polyomavirus Allograft Nephropathy: Sequential Assessment of Histologic Viral Load, Tubulitis, and Graft Function Following Changes in Immunosuppression

Çelik, Betül; Shapiro, Ron; Vats, Abhay; Randhawa, Parmjeet

doi:10.1046/j.1600-6135.2003.00238.x

Cited by 84 publications

(83 citation statements)

References 12 publications

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“…18 Moreover, it has been shown that an early diagnosis before the onset of clinically apparent nephropathy is associated with improved outcomes in this entity, which portends a poor prognosis. 2,19 The current practice in the management of PVAN involves the judicious manipulation of immunosuppression, 9,10 once the diagnosis has been confirmed by tissue biopsy. 2,7 However, insufficient decrement of immunosuppression prevents adequate disease control, whereas over reduction is associated with an increased risk of allograft rejection.…”

Section: Discussionmentioning

confidence: 99%

“…2,7 The cornerstone of PVAN management involves the reduction of immunosuppression in an attempt to restrain viral replication without inciting acute rejection. 9,10 Therefore, BKV DNA levels can guide the optimal level of immunosuppressive reduction and serve as a quantifiable surrogate marker of the course of infection. However, there appears to be limited data with regard to the presence and the level of BKV DNA in the plasma of renal transplant recipients without clinical evidence of PVAN.…”

Section: Introductionmentioning

confidence: 99%

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Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Chan¹,

Leung²,

Wong³

et al. 2012

Renal Failure

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Introduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine <155 μmol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 3-4-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (AE SD) level of viremia was 552.80 AE 1931.00 genome copies/mL, with 92.9% of patients having low levels of viremia corresponding to <1 Â 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Chan¹,

Leung²,

Wong³

et al. 2012

Renal Failure

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“…In their study, reduction in immunosuppression compared to pulse steroids was associated with reduction in cytopathic changes (83% vs. 20%; P=0.004) [53]. Pulse steroids did result in greater improvement in tubulitis (55% vs. 26%) but this effect was not associated with improvement in renal function.…”

Section: Management Of Biopsy Confirmed Bkvnmentioning

confidence: 88%

BK Virus Infection in Renal Allograft Recipients

Dadhania¹

2012

Current Concepts in Kidney Transplantation

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“…44,45 BKVN'de greft fonksiyon bozukluğu, kreatinin stabil seyretse bile tedaviye rağmen devam edebilir. 34,41,[46][47][48][49] Bunun yanında rejeksiyonun antilenfosit antikorlarla tedavisi de hastalığın ilerleyişini artırır. 49 Ayrıca, immünsupresyon tedavisinin değiştirilmesi ve azaltılması ile greft fonksiyonunda değişiklik olmadığını belirten yayınlar da vardır.…”

Section: Tarama Testleri̇unclassified

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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Polyomavirus Allograft Nephropathy: Sequential Assessment of Histologic Viral Load, Tubulitis, and Graft Function Following Changes in Immunosuppression

Cited by 84 publications

References 12 publications

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

BK Virus Infection in Renal Allograft Recipients

BK Nephropathy in Renal Transplant Patients: Review

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