11/35. BK polyomavirus interstitial nephritis in a renal allograft recipient.Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (bk virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for bk virus by electron microscopy.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
12/35. Renal allograft loss as the result of polyomavirus interstitial nephritis after simultaneous kidney-pancreas transplantation: results with kidney retransplantation.BACKGROUND: polyomavirus (PV) infection in kidney transplant patients has been reported to cause interstitial nephritis and subsequent graft loss. The cornerstone of current therapy is a reduction in immunosuppression, which can subsequently lead to kidney allograft rejection. This dilemma becomes even more challenging in the setting of simultaneous kidney-pancreas transplantation, because a reduction in immunosuppression may result in rejection of the pancreas allograft. Antiviral therapy has not been shown to be clinically successful in decreasing the risk of graft loss secondary to PV infection. Furthermore, because of limited experience, the decision to perform retransplantation in patients who lost their primary kidney grafts to PV interstitial nephritis becomes a difficult one. methods: Retrospective review and case studies. RESULTS: We report two successful living donor kidney retransplants in simultaneous kidney-pancreas transplant patients who lost their first kidney grafts to PV infection. Both patients are receiving rimantadine therapy and performing well, with functioning kidney and pancreas grafts and no evidence of recurrent PV interstitial nephritis 22 and 37 months after retransplantation. CONCLUSIONS: Although follow-up is limited, our initial experience would indicate that graft loss secondary to PV interstitial nephritis is not an absolute contraindication for kidney retransplantation.- - - - - - - - - - ranking = 3keywords = infection (Clic here for more details about this article) |
13/35. 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.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
14/35. polyomavirus infection and acute vascular rejection in a kidney allograft: coincidence or mimicry?During the past decade, polyoma virus (PV) infection has emerged as an important cause of graft dysfunction and failure in kidney transplant recipients. Establishing the correct diagnosis can be difficult, however, because the histologic appearance of PV infection can resemble acute cellular rejection. We report a kidney-pancreas transplant recipient with PV infection, in whom both vascular and cellular rejection were dominant histologic features in a renal biopsy specimen. The patient was successfully managed by tapering immunosuppressive therapy, and continues to have good graft function 3 years after diagnosis of PV infection. This case highlights the spectrum of inflammatory changes associated with PV infection, and the need for caution when such changes are attributed to rejection.- - - - - - - - - - ranking = 9keywords = infection (Clic here for more details about this article) |
15/35. 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.- - - - - - - - - - ranking = 2keywords = infection (Clic here for more details about this article) |
16/35. 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.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
17/35. polyomavirus simian virus 40 infection associated with nephropathy in a lung-transplant recipient.BACKGROUND: Between 1955 and 1963, millions of individuals worldwide received vaccines contaminated with polyomavirus simian virus (SV)40. Recent data suggest that some individuals may develop renal dysfunction related to SV40 infection, including individuals too young to have received contaminated vaccines. CASE REPORT AND RESULTS: Three years after bilateral lung transplantation, a 32-year-old man with cystic fibrosis developed nephrotic syndrome and progressed to end-stage renal failure over 1.5 years. He was shown to have nephropathy caused by SV40. The diagnosis was documented by detecting and confirming sequences of SV40 (but not BK or jc virus) in his kidney biopsy and urine by polymerase chain reaction, Southern blot, and dna sequencing. Positive immunohistochemistry for SV40 was found in his kidney, and neutralizing antibodies for SV40 were detected in his serum, before and after the onset of renal dysfunction. A source for the virus was not determined. His household contacts did not have serologic or molecular evidence of SV40 infection. No serum or tissue samples were available from his 27-year-old donor. DISCUSSION: This report shows that SV40 is circulating in the community and can cause nephropathy in transplant patients.- - - - - - - - - - ranking = 6keywords = infection (Clic here for more details about this article) |
18/35. Polyoma nephropathy and progressive multifocal leukoencephalopathy in a renal transplant recipient.Progressive multifocal leukoencephalopathy is a progressive and ultimately fatal white-matter disease of the brain that is associated with polyomavirus infection. It is uncommon in the general population, and even in the immunosuppressed patient, who is inherently at greatest risk for active infection with the virus, it is rare. The causative agent in progressive multifocal leukoencephalopathy, jc virus, has become increasingly important in recent years as its role in nephropathy in the renal transplant recipient has become better understood. We present a young renal transplant patient who developed nephropathy with renal biopsy changes consistent with polyomavirus lesions and then developed mental status changes and was diagnosed with progressive multifocal leukoencephalopathy.- - - - - - - - - - ranking = 2keywords = infection (Clic here for more details about this article) |
19/35. polyomavirus BK infection in Greek renal transplant recipients.BK polyoma virus associated nephropathy is increasingly recognized as an important cause of allograft dysfunction among renal transplant recipients. Herein we present the cases of two renal transplant recipients who developed progressive functional deterioration suspicious for BK polyoma virus involvement. One patient had been treated with mycophenolate mofetil (MMF), cyclosporine (CsA), and prednisolone (P), and the second patient with tacrolimus (Tac), MMF, and (P). Using quantitative real-time polymerase chain reactions for bk virus dna, we monitored the content of bk virus in the blood to evaluate disease progression. The high bk virus load initially detected in the blood samples from these patients decreased in the patient who received MMF, CsA, and P after the reduction of immunosuppression, but not in the patient who was treated with Tac, MMF and P. In contrast to previous reports, our patients had not received treatment with anti-lymphocyte globulin (ALG) or monoclonal anti-CD3 antibody (OKT3) after transplantation. It is concluded that even in the absence of vigorous antirejection treatment, immunosuppressive therapy based on Tac and MMF may carry the risk of bk virus-associated nephropathy. Because bk virus specific antiviral therapy is not available, its course may be monitored by measuring the viral load in blood.- - - - - - - - - - ranking = 4keywords = infection (Clic here for more details about this article) |
20/35. bk virus subtype 1 infection associated with tubulointerstitial nephritis in a renal allograft recipient.The BK polyomavirus (BKV) infects most of the human population, but clinically relevant infections are usually limited to individuals who are in an immunosuppressed state. The significance of BKV infection was investigated in a 50-year-old man who underwent cadaveric kidney transplantation and was treated with tacrolimus, mycophenolate mofetil and prednisolone. By staining renal biopsy specimens with a monoclonal antibody against BK large T antigen, we were able to observe the relationship between the appearance of the BKV antigen and the extent of immunosuppression in this patient. We also determined that BKV belonged to genotype I by analysis of viral dna from the patient's urine.- - - - - - - - - - ranking = 6keywords = infection (Clic here for more details about this article) |
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