Anterior Uveitis Associated With Treatment With Intravenous Cidofovir in Kidney Transplant Patients With BK Virus Nephropathy

López, Verónica; Sola, E.; Gutiérrez, Cristina; Burgos, D.; Cabello, Mercedes; García, Iván García; Flórez, Pablo; López, Javier; González‐Molina, Miguel

doi:10.1016/j.transproceed.2006.08.067

Cited by 33 publications

(22 citation statements)

References 8 publications

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“…Reports of the efficacy of treatment with adjuvant agents such as cidofovir, immunoglobulin, or quinolone class antibiotics have not been consistent [19][20][21][22][23][24][25][26]. Moreover, issues of toxicity, logistics of therapy, and expense limit the clinical application of these adjuvant agents [27][28][29]. Thus, reduction in immunosuppression currently is the mainstay of therapy for BK nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Monthly Screening for Polyoma Virus Eliminates BK Nephropathy and Preserves Renal Function

Petrov

Elbahloul

Gallichio

et al. 2009

Surgical Infections

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Section: Discussionmentioning

confidence: 99%

Monthly Screening for Polyoma Virus Eliminates BK Nephropathy and Preserves Renal Function

Petrov

Elbahloul

Gallichio

et al. 2009

Surgical Infections

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“…Cidofovir-associated uveitis is more common following intravitreal administration and typically occurs after multiple injections, with a mean of 4.2 injections in one study [11]. Although nearly all cases of cidofovir-associated uveitis occur in the eyes with a history of active or treated CMV retinitis, there is one report in a patient with non-ocular CMV [15] and a second report of 5 of 14 patients treated with low-dose intravenous cidofovir for polyomavirus-associated nephropathy [16]. The incidence of ocular side effects decreases significantly with concomitant administration of oral probenecid, with one study reporting a decrease from 71% to 18% [8].…”

Section: Reviewmentioning

confidence: 99%

“…Probenecid is believed to inhibit intraocular secretion of cidofovir from the ciliary body, thereby minimizing its intraocular concentration [13]. Previously, the pathogenesis of cidofovir-associated uveitis was hypothesized to be due to a direct reaction with the CMV; however, uveitis has been associated with the use of cidofovir in non-CMV-related viral infections as well [16]. …”

Section: Reviewmentioning

confidence: 99%

Drug-induced uveitis

London

Moorthy

Cunningham

2013

J OPHTH INFLAMM INFECT

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“…In a cohort of 21 recipients with BKV nephropathy, Kuypers et al (102) reported no graft loss in eight recipients who agreed to treatment with cidofovir but a 70% graft loss in the 13 who did not receive cidofovir. Cidofovir should be used with caution, frequent monitoring, and informed consent because of the potential complications (109,110). Quinolones, DNA gyrase inhibitors, may interfere with the large T antigen helicase activity (111) and have in vitro and in vivo activity against BKV (112)(113)(114).…”

Section: Adjuvant Therapiesmentioning

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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Anterior Uveitis Associated With Treatment With Intravenous Cidofovir in Kidney Transplant Patients With BK Virus Nephropathy

Cited by 33 publications

References 8 publications

Monthly Screening for Polyoma Virus Eliminates BK Nephropathy and Preserves Renal Function

Monthly Screening for Polyoma Virus Eliminates BK Nephropathy and Preserves Renal Function

Drug-induced uveitis

BK Virus Nephropathy and Kidney Transplantation

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