Cases reported "Tumor Virus Infections"

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1/28. Quantitation of bk virus load in serum for the diagnosis of bk virus-associated nephropathy in renal transplant recipients.

    bk virus-associated nephropathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, and definitive diagnosis requires renal biopsy. By using a newly developed, quantitative, real-time polymerase chain reaction (PCR) assay for bk virus dna, a retrospective analysis was done of sequential serum samples (n=28) from 4 transplant recipients with histopathologically documented bk virus nephropathy and from samples (n=76) from 16 transplant recipient control patients. bk virus dna was detected in serum samples from all 4 case patients versus 0 of 16 control patients (P< .0001, Fisher's exact test) at a median of 32 weeks (range, 17-61 weeks) before the diagnosis of bk virus nephropathy. bk virus load decreased in 3 of 3 patients after the reduction of immunosuppression and/or nephrectomy. It is concluded that quantitative PCR for bk virus dna in serum is useful both for identifying transplant recipients at risk for bk virus nephropathy and for monitoring the response to therapy.
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keywords = nephropathy
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2/28. polyomavirus BK nephropathy in a kidney transplant recipient: critical issues of diagnosis and management.

    diagnosis of polyomavirus BK nephropathy and treatment by low-dose immunosuppression may be optimized by using surrogate markers, such as the detection of viral inclusion bearing cells in the urine and polyomavirus BK dna in plasma by polymerase chain reaction. These markers were used prospectively in the management of a 44-year-old woman and led to the diagnosis of polyomavirus BK nephropathy at an early stage. The management was complicated by the concurrence of acute allograft rejection. Two treatment steps were initiated: antirejection therapy consisting of methylprednisolone for 3 days followed by lowering of the maintenance immunosuppression. This treatment resulted in a return of the serum creatinine concentration to the baseline of 1.6 mg/L, clearance of polyomavirus BK from plasma, and disappearance of viral inclusion bearing cells from the urine. After 2 months of stable allograft function, a control biopsy confirmed the resolution of polyomavirus BK nephropathy. Histologic signs of acute interstitial rejection were found and preemptively treated by methylprednisolone without altering the baseline regimen. Allograft function remained stable without evidence of recurrent polyomavirus BK nephropathy. This case shows the value of surrogate markers used in a prospective fashion for diagnosis and management of polyomavirus BK nephropathy with concurrent rejection.
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ranking = 1.125
keywords = nephropathy
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3/28. polyomavirus nephropathy in native kidneys of a solitary pancreas transplant recipient.

    BACKGROUND: Latent polyomavirus (PV) infection of the urinary tract can be reactivated by immunosuppression. When this occurs in the renal allograft, permanent loss of allograft function can occur. polyomavirus reactivation could potentially affect the native kidneys of nonrenal transplant recipients and cause renal dysfunction. methods: This article describes a case of PV nephropathy in the native kidneys of a solitary-pancreas transplant recipient. This patient had a progressive increase in serum creatinine. Screening urine cytology showed numerous cells with cytopathic changes suggestive of polyomavirus infection. RESULTS: biopsy of the native kidneys of this patient showed renal tubular cells with intranuclear inclusions characteristic of PV infection, which was confirmed by immunohistochemistry. Electron microscopy showed intranuclear viral particles. Patchy inflammation and fibrosis also were noted. CONCLUSION: polyomavirus reactivation can occur in the native kidneys of nonrenal solid organ transplant recipients. This should be considered in the differential diagnosis of renal impairment in these patients. The effects of PV reactivation on long-term native kidney function are not known.
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ranking = 0.625
keywords = nephropathy
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4/28. Prospective study of polyomavirus type BK replication and nephropathy in renal-transplant recipients.

    BACKGROUND: Nephropathy associated with the polyomavirus type BK (BKV) nephropathy has emerged as a cause of allograft failure linked to immunosuppressive regimens containing tacrolimus or mycophenolate mofetil. The presence of viral inclusions, known as "decoy cells," in urine and the presence of BKV dna in plasma have been proposed as markers for the replication of BKV and associated nephropathy, but data from prospective studies have been lacking. methods: In a prospective, single-center study, we followed 78 renal-transplant recipients who were receiving immunosuppressive therapy that included tacrolimus (37 patients) or mycophenolate mofetil (41 patients). urine was tested for the presence of decoy cells at routine visits. BKV dna was measured 3, 6, and 12 months after transplantation and whenever decoy cells were detected. The viral load in plasma was quantified with the use of a real-time polymerase-chain-reaction method. Renal biopsy was performed if allograft function deteriorated. RESULTS: Twenty-three patients had decoy-cell shedding a median of 16 weeks after transplantation (range, 2 to 69), 10 patients had BKV viremia at a median of 23 weeks (range, 4 to 73), and 5 had BKV nephropathy at a median of 28 weeks (range, 8 to 86). Kaplan-Meier estimates of the probability of decoy-cell shedding, viremia, and nephropathy were 30 percent (95 percent confidence interval, 20 to 40 percent), 13 percent (95 percent confidence interval, 5 to 21 percent), and 8 percent (95 percent confidence interval, 1 to 15 percent), respectively. Antirejection treatment, particularly with corticosteroids, was associated with BKV replication and nephropathy. The viral load in plasma was higher in patients with BKV nephropathy than in those without nephropathy (P<0.001 by the Mann-Whitney test). BKV antibodies were detected in 77 percent of the 78 patients before transplantation, including 4 of 5 with BKV nephropathy. CONCLUSIONS: BKV nephropathy in renal-transplant recipients represents a secondary infection associated with rejection and its treatment in most cases and could be monitored by measuring the viral load in plasma.
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ranking = 1.625
keywords = nephropathy
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5/28. De novo C1q nephropathy in the renal allograft of a kidney pancreas transplant recipient: bk virus-induced nephropathy?

    C1q nephropathy is a distinct entity characterized by extensive and dominant C1q mesangial deposition with associated steroid resistant proteinuria in the absence of systemic lupus erythematosus. Several morphological patterns ranging from very subtle glomerular alterations to focal/segmental glomerulosclerosis and mesangial proliferative changes have been described. Interstitial nephritis secondary to BK polyomavirus is a recently recognized complication in kidney transplant recipients. It may be associated with a tubulitis-like picture, mimicking sometimes acute tubular rejection. We report the case of a kidney pancreas transplant recipient who developed de novo C1q nephropathy, in the setting of BK polyomaviral interstitial nephritis. He presented with renal allograft dysfunction and a kidney biopsy was performed. It was interpreted as acute cellular rejection. C1q deposits were detected by immunofluorescence studies and electron microscopy. The patient did not respond clinically to appropriate anti-rejection treatment and a second renal biopsy was performed. The possibility of an interstitial nephritis secondary to BK polyomavirus mimicking rejection was suggested. Special immunohistochemical and blood/urine PCR studies for bk virus were performed, confirming the diagnosis of bk virus tubulonterstitial nephritis with a persistent, probable bk virus induced C1q nephropathy.
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ranking = 1.375
keywords = nephropathy
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6/28. Treatment of refractory bk virus-associated nephropathy with cidofovir.

    bk virus-associated nephropathy (BKVN) has become recognized as an important cause of allograft dysfunction in renal transplant recipients and despite reduction in immunosuppression, 30-40% of recipients ultimately progress to allograft loss. Cidofovir is an antiviral agent that demonstrates in vitro activity against murine polyomavirus and has been proposed for treatment of BKVN in renal allograft recipients. We describe the clinical course, renal function, serial renal histology and urine and blood viral load measurements in two consecutive patients with refractory BKVN who were treated with low-dose cidofovir (0.25 mg/kg IV). In each case, renal dysfunction and BK viral load progressed despite reduced immunosuppression, and persistent bk virus infection was documented in serial renal allograft biopsy specimens. Administration of low-dose cidofovir was associated with clearance of bk virus dna from blood and allograft, and stabilization of renal function in both patients, without significant toxicity. These preliminary data suggest that low-dose cidofovir may be tolerated, even among renal transplant recipients with significant renal dysfunction due to BKVN. Prospective, controlled trials are warranted to further define the optimal dose, toxicity and potential role of cidofovir in renal transplant recipients with bk virus nephropathy.
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ranking = 0.75
keywords = nephropathy
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7/28. infection with polyomavirus type BK after renal transplantation.

    Tubulointerstitial nephritis caused by polyomavirus of the subtype BK (bk virus nephropathy, BKN) is an important cause of deterioration of renal allograft function after kidney transplantation. In 3 cases of BKN diagnosed at our center, the suspected diagnosis made on the basis of urine cytology and serum PCR was confirmed by electron microscopy and immunohistology of the renal graft biopsy. In 1 patient, stable renal function without further virus detection was seen after reduction of the immunosuppression. In 2 further patients there was loss of graft function. BKN is an important differential diagnosis of unclear deterioration of renal graft function. The risk is particularly high with use of tacrolimus and mycophenolate mofetil (MMF). urine cytology and serum PCR are suitable screening tests, histology provides conclusive evidence. The only therapeutic option available at present is reduction of immunosuppressive therapy.
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ranking = 0.125
keywords = nephropathy
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8/28. Retransplantation after kidney graft loss due to polyoma bk virus nephropathy: successful outcome without original allograft nephrectomy.

    Although polyoma bk virus (BKV)-associated interstitial nephritis has received increasing attention because of its clinical relevance in kidney allograft recipients, data on risk for repeated renal transplantation after BKV-related allograft loss are limited, and the need to perform an original graft nephrectomy is the object of debate. A 15-year-old boy with renal failure secondary to Alport's syndrome underwent renal transplantation. His posttransplantation course was complicated by acute rejection episodes and the presence of circulating anti-glomerular basement membrane antibodies that required aggressive immunosuppressive treatment. Graft failure caused by BKV-associated interstitial nephropathy occurred despite a reduction in immunosuppression and cidofovir treatment. The patient received a second transplant without an original graft nephrectomy, and 15 months after retransplantation, he persists with optimal graft function and is constantly BKV dna negative in both urine and plasma. Our report indicates that an original allograft nephrectomy may not be mandatory for successful retransplantation after graft loss caused by BKV nephropathy.
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ranking = 0.75
keywords = nephropathy
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9/28. CMV and BKV ureteritis: which prognosis for the renal graft?

    This report describes two cases of ureteral stricture in renal graft recipients related to cytomegalovirus (CMV) and human polyoma bk virus (BKV) ureteritis with the same onset characterized by acute graft failure with no clinical signs of systemic viral infections. The histological analysis did not show other causes of graft impairment (i.e. drug toxicity and acute rejection). Ultrasound scan (US) revealed absent or mild hydronephrosis. The diuretic-MAG3 renal scan showed a urinary flow obstruction. The viral genomes were isolated from urine, peripheral blood and graft or ureteral tissues samples. A percutaneous nephrostomy confirmed the stricture, but it restored urine flow only in the graft affected by CMV ureteritis, the association with a specific antiviral therapy probably produced a stable restoration of graft function. In BKV ureteritis,the graft prognosis was poor; graft loss could be due to the progress of BKV nephropathy. A correct differential diagnosis of the etiologic agent responsible for the ureteritis is mandatory, because treatment and outcome of the infection are different.
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ranking = 0.125
keywords = nephropathy
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10/28. association of renal adenocarcinoma and bk virus nephropathy post transplantation.

    While most bk virus infections are asymptomatic, immunosuppression has been associated with bk virus reactivation and impaired graft function or ureteric ulceration in renal transplant patients and hemorrhagic cystitis in bone marrow transplant patients. Oncogenicity is also postulated and this is the first report of a child with a carcinoma of the donor renal pelvis following bk virus allograft nephropathy. Removal of the primary tumor and cessation of immunosuppression led to regression of secondary tumors and a return to health.
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ranking = 0.625
keywords = nephropathy
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